My brother Ben is now a respectable consultant for the Oxford English Dictionary, but when he was a kid, he was a puzzle freak, pure and simple. In fourth grade he'd spend hours paging through a big unabridged Webster's, looking for obscure words that he could use to create a fiendish rebus. Little did I know that one day one of his favorite puzzles--the doublet--would become useful to me in thinking about evolution.

The challenge of a doublet is to turn one word into another. You are allowed to change one letter at a time, but each change must produce a real word. Here's a doublet that suits a post on evolution: Change APE to MAN.

Give up?

APE

APT

OPT

OAT

MAT

MAN

Now imagine that having solved the APE-to-MAN puzzle, you tell a friend about your triumph.

Your friend scoffs. "That's ridiculous," he says. "I don't believe you've found a missing link between APE and MAN. It doesn't exist."

You furrow your brow. "Wait," you say. "No, I think maybe you didn't hear how the puzzle works--"

"I mean, what comes in between?"

"Well, there's APT, and then--."

"APT? Please! That's nothing like MAN. They don't have a single letter in common. It's just a completely separate word on its own."

"But then there's OPT--"

"OPT? Are you kidding me? That's just as irrelevant. You can't just go from APE to MAN through OPT."

"But what about MAT? That's a lot like MAN."

"Sure," your friend says, rolling his eyes. "But what on Earth does it have to do with APE?"

Is he really not getting it, you might ask yourself, or is he just pretending not to understand what I'm saying? That's how I felt when someone sent me an email to tip me off about an attack at the creationist web site Answers in Genesis. It is based on either a misunderstanding or a misrepresentation of what evolution is all about. And doublets help to explain why.

The attack concerns an interview I gave recently to an Australian radio talk show. The Aussies called me up to talk about President Bush's endorsement of discussing Intelligent Design in schools. Along the way, I explained why creationism has failed to win support in the scientific community. For one thing, creationists often base their arguments on supposed gaps in evolution, such as "missing links" in the fossil record. I talked about how creationists used to talk about the absence of intermediate fossils that would show how whales had evolved from land mammals. But once paleontologists began to find walking whales, the creationists no longer made that argument, moving on to some other gap.

I guess the creationists in Australia were listening to me that day, because now Mark Looiy of Answers in Genesis is here to tell you that in fact "creationists have been devoting many a printed (and web) page—and public lectures—to assertively debate the evolutionary whale claim."

Let's set aside the fact that scientific debates take place at conferences of scientific societies or in the pages of peer-reviewed biology journals. What exactly are the creationists offering in these pages and lectures? They claim that the fossils of early whales don't support the argument that whales evolved from land mammals, but their claims are unfounded for a number of reasons.

For one thing, Looiy's article (and a book by Jonathan Sarfati that he links to as evidence that creationists are still on the whale evolution case) are simply riddled with factual errors. To choose just one example, Sarfati claims that the fossil of Ambulocetus, an alligator-like whale with big feet, is "(conveniently) missing" the pelvis and other parts that are supposedly crucial to establishing the transition from land to sea. I imagine here a paleontologist gasping at the sight of a pelvis that disprove evolution and smashing it with his rock hammer. In fact, Hans Thewissen, the paleontologist who discovered Ambulocetus in Pakistan, has gone back year after year and has now found its pelvis and almost every other bone in this creature. And the complete skeleton supports his initial conclusion that this whale used its legs to kick through the water like an otter.

But there's a more fundamental problem with Looiy and Sarfati's take on whales. They look at individual fossils of whales and declare that each one tells us nothing about how whales evolved into marine mammals. The oldest whale, the goat-like Pakicetus, had fully terrestrial legs, so it tells us nothing. Much later, the fully aquatic whale Basiolosaurus retained tiny legs complete with ankles, but since it was completely marine, it also tells us nothing.

What they either don't know or don't want to explain is that scientists reconstruct evolutionary history by looking not at one species, but as many species as they can. They draw evolutionary trees by analyzing fossils or DNA, and they look at the traits that are shared by species on different branches of the tree. Pakicetus does look to have been very terrestrial, but it also had peculiar structures in its skull that are only found in whales. Over time, whale legs appear to have changed as whales adapted to the water--first becoming otter-like in the case of Ambulocetus, and then more seal-like in the case of Rodhocetus. Basilosaurus was much further along in this evolution, with much reduced legs that offered no help in swimming at all. And today, whales carry vestiges of hips.

No one species bridged the entire transition from land mammal to marine whale, just as no word bridges the transition from APE to MAN. What's more, many of these early whale fossils--while related to living whales--did not give rise to them directly. They're more like aunts and uncles to today's living whales. In some cases, such as a group called remingtonocetids, walking whales branched off in weird directions of their own, in some cases evolving bizarre heron-shaped heads. A couple years ago Thewissen summarized all the information available on fossil and living whales with this tree--a tree that continues to support the evolution of whales from terrestrial ancestors. It may not be the full solution to the doublet LAND MAMMAL to MARINE WHALE, but it's a very good start.

"March of the Penguins," the conservative film critic and radio host Michael Medved said in an interview, is "the motion picture this summer that most passionately affirms traditional norms like monogamy, sacrifice and child rearing." --from an article describing how some religious leaders and conservative magazines are embracing the blockbuster documentary.

Well, it's 2010, and what a remarkable five years it's been. The blockbuster success of March of the Penguins in 2005 triggered a flood of wonderful documentaries about animal reproduction, all of which provide us with inspiring affirmation of the correct way to live our lives. Here are just a few of the movies that can guide you on your path...

Dinner of the Redback Spiders: This documentary follows the heartwarming romance between two spiders that ends with the male somersaulting onto the venomous fangs of his mate, his reproductive organs still delivering semen into the female as she devours him.

Toxic Love of the Fruit Flies: In this movie, male fruit flies demonstrate their ingenuity and resourcefulness by injecting poisonous substances during sex that make it less likely that other males will successfully fertilize the eggs of their mates. Sure, these toxins cut the lifespan of females short, but who said life was perfect?

Harem of the Elephant Seals: Meet Dad: a male northern elephant seal who spends his days in bloody battles with rivals who would challenge his right to copulate with a band of females--but doesn't life a finger (or a flipper) to help raise their kids.

Step-fathers of the Serengeti: Guess who's moving in? It's a male lion taking over a pride of females. Watch him affirm traditional norms by killing their cubs so that they can father his own offspring.

Funky Love of the Bonobos: The sexual shenanigans of some of our closest living ape relatives. Male-female, female-female, and on and on it goes. Warning: Definitely not suitable for children.

(Warning: this post contains some journalistic/blogging inside-baseball material.)

Back in the dark ages (otherwise known as the 1990s), writing about science felt a bit like putting messages in a bottle. I'd write an article, a few weeks or months later it would appear in a magazine, and a few weeks or months later I might get a response from a reader. In some cases, an expert might point out an error I made. In other cases, she or he might explain the real story which I had missed. The delay could make for some disconcerting experiences. The first time I met the late Stephen Jay Gould, to interview him for a book I was working on, I was still lowering myself into a chair when he began complaining about the cover headline to a story I had written about fossil birds over a year beforehand. I stared at him blankly for a while as I reached back into my memory banks to figure out what he was talking about.

It's much better these days, now that people can hammer me with emails seconds after my stories is are published. Science is a murky, complex endeavor, and my job has never stopped feeling like an apprenticehip, as I learn from mistakes.

But this new arrangement comes with a downside. Some criticisms are unjustified, and instead of simply emailing me these complaints, people sometimes decide to publish them for all to see.

John Hawks, an anthropologist at the University of Wisconsin, has done just this. He has written a long complaint about an article I wrote for the latest issue of Discover. The issue celebrates the 25th anniversary of the magazine, and it contains a series of two-page spreads that take a look at different fields in science and where they're headed. The editors asked me to contribute a piece on human evolution. I included an interview with Tim White of Berkeley, an essay on the growing role of scanning in studies on hominid fossils, and a large graphic showing how scientists used CT-scans to reconstruct the skull of Sahelanthropus, the oldest known skull of a hominid.

Hawks makes a series of complaints about the piece, but rather than sticking to the article itself, he tends to focus on the "subtext," which he alone has the mysterious power to read. For example, the subtext apparently says that "anything high tech must be better." I never made such a claim, and it would have been silly for me to add a disclaimer to that effect: "Warning--not all things high tech are better." Healthy skepticism is certainly a virtue, but Hawks is ignoring the fact that the entire issue is dedicated to promising new scientific developments. (Here's an article on research on using lasers in art conservation. I suppose Hawks would complain that the article didn't mention that lasers can also kill people.)

When Hawks does actually deal with the article itself, he makes some serious mistakes. He mocks the conclusion of my piece, in which I describe some new applications of fossil scans--such as reconstructing wounds, simulating hominids walking, and making the scans available online to other researchers who can't see the originals. "So utopian," he sneers.

As evidence, he turns to my interview with Tim White, in which White talked about the importance of other kinds of technology to the study of human evolution--such as the global positioning system, advances in dating fossils. "No CT scans there," Hawks declares.

Hawks shouldn't argue from the absence of evidence. Actually, White talked to me at length about the promise of CT scans, including some of the applications I mentioned in the article. It would have been redundant to include his comments. Hawks may not be impressed by scans, but he shouldn't count White on his side.

So why isn't Hawks impressed with scans? For one thing, scientists can make mistakes with them, producing recontructions as biased as any handmade reconstruction. "The principle of 'garbage in, garbage out' is everlasting," he says.

True, but so what? I remember the same argument being made in the 1990s, when some biologists were starting to reconstruct the tree of life by using computers to analyze DNA sequences and morphological features, rather than relying on a more intuitive sense of what evolved from what (a method known as cladistics). Critics warned that the cladists were just dumping bad data into their computers, and so their conclusions couldn't be trusted. In fact, the cladists were producing testable hypotheses with explicit assumptions that anyone could challenge. Of course there are cases in which this approach may face problems (in comparing populations of the same species, for example, or species that can swap genes, for example). But that hasn't stopped cladistic trees from becoming the standard for the field. The garbage-in-garbage-out complaint is equally beside the point when it comes to predicting the importance of scans to the study of human evolution.

Descending again into my subtext, Hawks writes that "a read of the article gives the impression that every finding from this new advanced technology supports splitting hominids into several species." If I may indulge in a little subtext-divining myself, I think we're getting somewhere now. Hawks is a long-time proponent of the idea that too many hominid fossils have been designated as separate species. It just so happens that a couple of recently published scans--one of Neanderthal children and one of the "Hobbit" brain--have been interpreted by the authors of these studies as supporting the idea that these fossils do not belong to humans, but to other species. But instead of directing his wrath at these scientists, Hawks directs it at me. In order to do so, however, he has to ignore the fact that I write about many other applications of scans that don't support splitting hominids into several species.

Hawks is perfectly entitled to attack hominid-splitting (and on his blog he has done a great job of documenting new research that supports his attack). But I don't appreciate him distorting my own writing to serve that agenda. It's particularly unfair to do so when most people haven't had a chance to read the article for themselves, and have to rely instead on Hawks's misleading summary.

Update, Wed. 1pm: Another improvement on the dark ages: when I attack, the attackee can respond. John Hawks defends his post in the comments. I agree that CT scans of hominid fossils are not now being freely shared on the net. But I think there's reason to be optimistic--see, for example, the Digimorph Project, which is building up a big database of scans of bones from living and fossil animals. Would it have been utopian to predict Digimorph a decade ago?

I'm back from a computer-free vacation, and of course I have returned to mountains of emails and a long chain of fascinating new links. In place of any original thoughts of my own, let me just point you to a few things that look interesting (if you have any mental space not presently occupied by the horrors of Katrina).

1. Over the past couple years I've enjoyed watching Chris Mooney's blogging and articles evolve into a full-blown book, The Republican War on Science, which has just come out. Tonight he hits the big time tonight on the Daily Show.

2. Mooney is actually just part of the opening night of a week-long evolution series on the Daily Show. A couple years ago my wife and I decided to give up cable because we feared we'd be use up what little free time we had watching has-been celebrity biographies or movies about evil mechanical sharks. (I should point out that my wife is strangely immune to the lure of the mechanical sharks.) It's times like these, though, when I wish we still had just a little cable.

3. Human brains are evolving. Questionable Authority recaps. Will Bruce Lahn get the Nobel Prize someday?

4. Parasites are manipulating. Latest case: grasshoppers hurling themselves to their death on behalf of hairworms. Not a public health threat like malaria's sweet perfume, but very high on the science-fiction-meter.

5. Life on Titan? Astronomer David Grinspoon thinks all the raw ingredients are there.

Clint, the chimpanzee in this picture, died several months ago at a relatively young age of 24. But part of him lives on. Scientists chose him--or rather, his DNA--as the subject of their first attempt to sequence a complete chimpanzee genome. In the new issue of Nature, they've unveiled their first complete draft, and already Clint's legacy has offered some awesome insights into our own evolution.

The editors of Nature have dedicated a sprawling space in the journal to this scientific milestone. The main paper is 18 pages long, not to mention the supplementary information kept on Nature's web site. In addition, the journal has published three other papers that take a closer look at particularly interesting (and thorny) aspects of the chimpanzee genome, such as what it says about the different fates of the Y chromosome (the male sex chromosome) in chimpanzees and humans. Other scientists offer a series of commentaries on topics ranging from brain evolution to chimpanzee culture. The journal Science has also gotten in on the action, with a paper comparing the expression of chimp and human genes as well as comments on the importance of chimpanzee conservation and research. (Thankfully, some of this material is going to be made available online for free.)

Why all the attention to the chimpanzee genome? One important reason is that it can tell us what parts of the human genome make us uniquely human--in other words, which parts that were produced by natural selection and other evolutionary processes over the past six million years or so, since our hominid ancestors diverged from the ancestors of our closest living relatives, chimpanzees. (Bonobos, sometimes known as pygmy chimpanzees, are also our first cousins, having split off from chimpanzees 2-5 million years ago.) Until now, scientists could only compare the human genome to the genomes of more distantly related species, such as mice, chickens, and fruit flies. They learned a lot from those comparisons, but it was impossible for them to say whether the differences between humans and the other species were unique to humans, or unique to apes, or to primates, or to some broader group. Now they can pin down the evolutinary sequence much more precisely. Until scientists rebuild the Neanderthal genome--if they ever do--this is going to be the best point of comparison we will ever get. (For more of the background on all this, please check out my new book on human evolution, which will be out in November.)

The analysis that's being published today is pretty rudimentary. It's akin to what you'd expect from a reporter who got to spend an hour flipping through 10,000 pages of declassified government documents. But it's still fascinating, and I'd wager that it serves as a flight plan for research on the evolution of the human genome for the next decade.

First off, scientists can get a more precise figure of how different human and chimpanzee DNA is. In places where you can line up stretches of DNA precisely, there are 35 million spots where a single "letter" of the code (a nucleotide) is different. That comes to about 1.2% of all the DNA. The scientists also found millions of other spots in the genomes where a stretch of DNA had been accidentally deleted, or copied and inserted elsewhere. This accounts for about a 3% difference. Finally, the scientists found many genes that had been duplicated after the split between humans and chimps, corresponding to 2.7% of the genome.

By studying the human genome, scientists have also gotten a better picture of the history of the genomic parasites that we carry with us. About half of the human genome consists of DNA that does not produce proteins that are useful to our well-being. All they do is make copies of themselves and reinsert those copies at other spots in the genome. Other animals have these virus-like pieces of DNA, including chimpanzees. Some of the genomic parasites we carry are also carried by chimpanzees, which means that we inherited them from our common ancestor. Many of these parasites have suffered mutations that make them unable to copy themselves any longer. But in some cases, these parasites have been replicating (and evolving) much faster in one lineage than the other. One kind of parasite, called SINES, have spread three times faster in humans than in chimps. Some 7,000 genomic parasites known as Alu repeats exist in the human genome, compared to 2,300 in the chimp genome. While a lot of these parasites have no important effect on our genome, others have. They've helped delete 612 genes in humans, and they've combined pieces of some 200 other genes, producing new ones.

In some cases, the interesting evolution has occurred in the chimpanzee lineage, not in our own ancestry. Scientists have noted for a long time that the Y chromosome has been shrinking for hundreds of millions of years. Its decline has to do with how it is copied each generation. Out of the 23 pairs of our chromosomes, 22 have the same structure, and as a result they swap some genes as they are put into sperm or egg cells. Y chromosomes do not, because their counterpart, the X, is almost completely incompatible. My Y chromosome is thus a nearly perfect clone of my father's. Mutations can spread faster when genes are cloned than when they get mixed together during recombination. As a result, many pieces of the Y chromosome have disappeared over time, and many Y genes that once worked no longer do.

Scientists have discovered that Clint and his fellow chimpanzee males have taken a bigger hit on the Y than humans have. In the human lineage, males with mutations to the Y chromosome have tended to produce less offspring than those without them. (This is a process known as purifying selection, because it strips out variations.) But the scientists found several broken versions of these genes on the chimpanzee Y chromosome.

Why are chimpanzees suffering more genetic damage? The authors of the study suggest that it has to do with their sex life. A chimpanzee female may mate with several males when she is in oestrus, and so mutations that give one male's sperm an edge over other males are ben strongly favored by selection. If there are harmful mutations elsewhere on that male's Y chromosome, they may hitchhike along. We humans are not so promiscuous, and the evidence is in our Y chromosome.

As for the mutations that make us uniquely human, the researchers point out some suspects but make no arrests. The researchers found that a vast number of the differences between the genomes are inconsquential. In other words, these mutations didn't have any appreciable effect on the structure of proteins or on the general workings of the human cell. But the scientists did identify a number of regions of the genome, and even some individual genes, where natural selection seems to have had a major impact on our own lineage. A number of these candidates support earlier studies on smaller parts of the genome that I've blogged about here. Some of these genes appear to have helped in our own sexual arms race; others created defenses against malaria and other diseases.

When scientists first lobbied for the money (some twenty to thirty million dollars) for the chimp genome project, they argued that the effort would yield a lot of insight into human diseases. The early signs seem to be bearing them out. In their report on the draft sequence, they show some important genetic differences between humans and chimpanzees that might have bearing on important questions such as why we get Alzheimer's disease and chimps don't and why chimpanzees are more vulnerable to sleeping sickness than we are, and so on.

There is also a lot of variation within our own species when it comes to disease-related genes, and here too the chimpanzee genome project can shed light. The researchers show how some versions of these genes found in humans are the ancestral form also shared by chimpanzees. New mutations have arisen in humans and spread in the recent past, possibly favored by natural selection. The ancestral form of one gene called PRSS1, for example, causes pancreatitis, while the newer form does not.

But our genetic defenses and weaknesses to diseases aren't really what we'd like to think make us truly, uniquely human. The most profound difference between the bodies of humans and chimpanzees is the brain. Much of the evolution that's been going on in genes expressed in the brain has been purifying. There are a lot of ways to screw up a brain, in other words. But some genes appear to have undergone strong positive selection--in other words, new mutation sequences have been favored over others. It's possible that relatively few genes played essential roles in producing the human brain.

You can feel the excitement of discovery thrumming through these papers, but it comes with a certain sadness as well. It doesn't come just from the fact the chimpanzee whose DNA made this all possible died before he became famous. Lots of chimpanzees are dying--so many, in fact, that conservationists worry that they may become extinct from hunting, disease, and habitat destruction. And once a species is gone, it takes a vast amount of information about evolutionary history with it.

I was reminded of this fact when I read another chimpanzee paper that appears in the same issue of Nature, reporting on the first fossil of a chimpanzee ever discovered. It may be hard to believe that no one had found a chimp fossil before. A big part of the problem, scientists thought, was that chimpanzees were restricted to rain forests and other places where fossils don't have good odds of surviving. The fossils that have now been discovered don't amount to much--just a few teeth--and they raise far more questions than they answer. They date back about 500,000 years, to an open woodlands in Kenya where paleoanthropologists have also found fossils of tall, big-brained hominids that may have been the direct ancestors of Homo sapiens. So apparently chimpanzees once coexisted with hominids in the open woodlands that were once thought to be off-limits to them. More chimpanzee fossils will help address this puzzle, but they may never fully resolve it.

The chimpanzees of Kenya became extinct long ago, and now other populations teeter on the brink. To make sense of Clint's genome, scientists need to document the variations both within and between chimpanzee populations--not just genetic variations, but variations in how they eat, how they organize their societies, how they use tools, and all the other aspects of the lives. If they don't get that chance, the chimpanzee genome may become yet another puzzling fossil.

Our genes are arrayed along 23 pairs of chromosomes. On rare occasion, a mutation can change their order. If we picture the genes on a chromosome as

ABCDEFGHIJKLMNOPQRSTUVWXYZ

a mutation might flip a segment of the chromosome, so that it now reads

ABCDEFGHISRQPONMLKJTUVWXYZ

or it might move one segment somewhere else like this:

ABCDLMNOPQRSTUEFGHIJKVWXYZ

In some cases, these changes can spread into the genome of an entire species, and be passed down to its descendant species. By comparing the genomes of other mammals to our own, scientists have discovered how the order of our genes has been shuffled over the past 100 million years. In tomorrow's New York Times I have an article on some of the latest research on this puzzle, focusing mainly on two recent papers you can read here and here.

One of the most interesting features of our chromosomes, which I mention briefly in the article, is that we're one pair short. In other words, we humans have 23 pairs of chromosomes, while other apes have 24. Creationists bring this discrepancy up a lot. They claim that it represents a fatal blow to evolution. Here's one account, from Apologetics Press:

If the blueprint of DNA locked inside the chromosomes codes for only 46 chromosomes, then how can evolution account for the loss of two entire chromosomes? The task of DNA is to continually reproduce itself. If we infer that this change in chromosome number occurred through evolution, then we are asserting that the DNA locked in the original number of chromosomes did not do its job correctly or efficiently. Considering that each chromosome carries a number of genes, losing chromosomes does not make sense physiologically, and probably would prove deadly for new species. No respectable biologist would suggest that by removing one (or more) chromosomes, a new species likely would be produced. To remove even one chromosome would potentially remove the DNA codes for millions of vital body factors. Eldon Gardner summed it up as follows: “Chromosome number is probably more constant, however, than any other single morphological characteristic that is available for species identification” (1968, p. 211). To put it another way, humans always have had 46 chromosomes, whereas chimps always have had 48.

There's a lot that's wrong here, and it can be summed up up with one number: 1968.

Why would someone quote from a 37-year-old genetics textbook in an article about the science of chromosomes? It's not as if scientists have been just sitting around their labs since then with their feet up on the benches. They've been working pretty hard, and they've learned a lot. And what they've learned doesn't agree with what Apologetics Press wants to claim.

The first big discovery came in 1982, when scientists looked at the patterns of bands on human and ape chromosomes. Chromosomes have a distinctive structure in their middle, called a centromere, and their tips are called telomeres. The scientists reported that the banding pattern surrounding the centromere on human chromosome 2 bore a striking resemblance to the telomeres at the ends of two separate chromosomes in chimpanzees and gorillas. They proposed that in the hominid lineage, the ancestral forms of those two chromosomes had fused together to produce one chromosome. The chromosomes weren't lost, just combined.

Other researchers followed up on this hypothesis with experiments of their own. In 1991, a team of scientists managed to sequence the genetic material in a small portion of the centromere region of chromosome 2. They found a distinctive stretches of DNA that is common in telomeres, supporting the fusion hypothesis. Since then, scientists have been able to study the chromosome in far more detail, and everything they've found supports the idea that the chromosomes fused. In this 2002 paper, for example, scientists at the Fred Hutchinson Cancer Research Center reported discovering duplicates of DNA from around the fusion site in other chromosomes. Millions of years before chromosome 2 was born, portions of the ancestral chromosomes were accidentally duplicated and then relocated to other places in the genome of our ancestors. And this past April, scientists published the entire sequence of chromosome 2 and were able to pinpoint the vestiges of the centromeres of the ancestral chromosomes--which are similar, as predicted, to the centromeres of the corresponding chromosomes in chimpanzees.

Today geneticists sometimes encounter people with fused chromosomes, which are often associated with serious disorders like Downs syndrome. But that doesn't mean that every fusion is harmful. Many perfectly healthy populations of house mice, for example, can be distinguished from other house mice by fused chromosomes. The fusion of chromosome 2 millions of years ago may not have caused any big change in hominid biology--except, perhaps, by making it difficult for populations of hominids with 23 pairs of chromosomes to mate with populations who still had 24. As a result, it may have helped produce a new species of hominid that would give rise to our own.

Just goes to show what 37 years of scientific research can turn up.

Update: Tuesday, 3:30: Thanks to Dr. Paul Havlak for pointing out that some people with fused chromosomes suffer no ill effects. This site at the University of Utah has more information.

Sometimes a picture can tell you a lot about evolution. This particular picture has a story to tell about how two species--in this case a fly and an orchid--can influence each other's evolution. But the story it tells may not be the one you think.

Coevolution, as this process is now called, was one of Darwin's most important insights. Today scientists document coevolution in all sorts of species, from mushroom-farming ants to the microbes in our own gut. But Darwin found inspiration from the insects and flowers he could observe around his own farm in England.

Darwin's thoughts about coevolution began with a simple question: how do flowers have sex? A typical flower grows both male and female sexual organs, but Darwin doubted that a single flower would fertilize itself very often. Flowers, like other organisms, display a lot of variation, and Darwin thought that the only way flowers could vary was if individuals mates, mixing their characters. (Sex turns out not essential for creating variation, but it does do a good job of creating it.) But in order to have sex, plants can't walk around to find a mate. Somehow the pollen of one flower has to get to another. Not just to any flower, moreover, but to a member of its own species.

The random wind might suffice for some plants. But Darwin also knew that bees visited many flowers to gather their nectar. He began to study what happened on those visits. He would watch bees land on scarlet kidney bean plants, for example, and climb up a petal to get to its nectar. The flower's pollen-bearing organs, Darwin found, were located in precisely the right spot to brush pollen onto the back of feeding bees. When the bees traveled to another scarlet kindey bean plant, they unloaded the pollen. The bees depended on the flowers for food, and the flowers depended on the bees for sex. Without each other, they could not survive.

In the Origin of Species, Darwin offered some thoughts on how this sort of partnership between bees and clover could have evolved. Imagine that the flowers are pollinated by other insects, but the insects go extinct in some region. Now all their nectar goes uneaten. Honeybees might visit the flowers sometimes, and variations that allowed them to reach the nectar--a longer tongue-like proboscis, for example, more easily might be favored by natural selection.

Meanwhile, the flowers would be experiencing intense natural seleciton of their own. Without their old pollinators, their chances of producing offspring plummeted. Any variation that would make it easier for honeybees to pollinate them would bring a huge increase in reproductive success. Gradually, the flowers anatomy would come to match that of the honeybees, just as the honeybees were adapting to the flower.

 "Thus I can understand," Darwin wrote, "how a flower and a bee might slowly become, either simultaneously or one after the other, modified and adapted in the most perfect manner to each other, by continued preservation of individuals presenting mutual and slightly favoruable deviations of structure." 

Around the time that Darwin published the Origin of Species, he developed a fondness for orchids. He was not alone; at the time a rising orchid fever was seizing England's upper class. Aristocrats would dispatch explorers to the Amazon or to Madagascar, where they would strip entire hillsides of the rare plants. Some prized specimens sold for hundreds of pounds at auctions in London and Liverpool. If, as many people then believed, the only meaning of natural beauty was as a gift from God, orchids were the most exquisite gifts of all. They could have only one purpose: to please the eye of man.

Darwin had other ideas.

In orchids, he discovered the same evolutionary pressures at work as in other flowers, but the results were supremely baroque and bizarre. Despite the prices orchids might fetch at auction, their beauty did not exist for beauty's sake. It was, Darwin showed, an elaborate means for luring insects into their sex lives. He documented case after case of these adaptations. One species, for example, had its pollen loaded in a crossbow-like structure that bees triggered by walking across a petal.

Darwin described this and many other adaptations in The Various Contrivances by Which British and Foreign Orchids are Fertilized by Insects, and on the Good Effects of Intercrossing. Darwin guided the reader from orchid to orchid, showing how each flower's design was not simply beauty for beauty's sake, but some of nature's most elaborate forms of sex. He showed how orchids were simply highly evolved flowers. All the various parts of ordinary flowers had simply been stretched and twisted and otherwise transmogrified into new structures such as crossbows.

Darwin was so confident that orchids were adapted to their pollinators that he made a bold prediction in his book. He pointed out how many orchids produce their nectar at the bottom of long tubes called nectaries. The insects that feed on them are equipped with tongues that are almost the same length. Short-tongued insects visit flowers with shallow nectaries, and long-tongued insects visit deep nectaries. In every case, the insect has to press its head against the flower to reach the bottom of the tube. The orchid's pollen is invariably positioned in a place where it can stick to the insect's head while it drinks.

Darwin saw the evolution of these tubes and tongues as the result of a race between flower and insect. If an insect could drink nectar without pressing its head against the orchid, it couldn't pass on its pollen. Natural selection would thus favor orchids with longer tubes. At the same time, an insect with a tongue that was too short for the tube wouldn't be able to drink all the nectar.

In some cases, this race between orchid and insect might drive each partner to absurd extremes. Darwin once received an orchid from Madagascar, called Angraeceum sequipedale, with a whip-shaped nectary over eleven inches long, with a drop of nectar tucked away at its very base. Only an animal with a suitably long tongue could drink it. Darwin predicted that somewhere in Madagascar there must live just such an insect.

The orchid's pollen, he declared, "would not be withdrawn until some huge moth, with a wonderfully long proboscis, tried to drain the last drop."

When Darwin died in 1882, the Madagascar orchid was still without a partner. But in 1903 entomologists discovered an extraordinary Madagascar hawkmoth. Normally its proboscis remained curled up like a watch spring. But when it approached orchids, it pumped fluid into the proboscis to straighten it out like a party balloon, and then insert it into the flower, as carefully as a tailor threads a needle's eye.

Scientists have found many other orchids and other flowers with an equally intimate relationship with their pollinators. Steven Johnson, a South African biologist, has documented lots of them in his part of the world, as he descirbed in an excellent article this spring in Natural History.

Now, in the August issue of the American Journal of Botany, Johnson and his colleagues have published a paper about a new orchid, shown in this picture. Disa nivea is a rare orchid found only in a few places in South Africa, and until Johnson came to study it, no one knew how it was pollinated. After a lot of patient orchid-watching, he and his colleagues discovered that it is visited exclusively by the fly shown in the picture. Its proboscis is well-matched to the length of the orchid, and the orchid grows pollen in just the right place so that they get stuck to the fly. You can see them in this picture--the two dangling yellow packets on the fly's snout.

There's just one catch: when the fly manages to get its proboscis all the way down to the bottom of the orchid's nectary, it finds no nectar.

To explain this deceit, Johnson and his colleagues observe that the orchids are always found intermingled with a similar-looking plant related to foxgloves. These plants are also pollinated by the same fly, but unlike the orchid, they reward visiting flies with nectar. Johnson and his colleagues argue that the orchid has evolved to mimic the rewarding flower, luring the flies with the same cues but deceiving them in the end.

To test this hypothesis, the scientists looked at five populations of the rewarding flower, measuring their dimensions. They found that from one population to another, the orchids mimic their local models. In some places, the rewarding flower is twice as long as in other places; the same goes for the orchid. Where the rewarding flowers are wide, so are the orchids; where they are narrow, the orchids are as well. These patterns are evidence that the evolution of this deceit is not a thing in the past, but an ongoing process.

Darwin would have not believed that such a deceitful plant could exist. Botantists had reported nectarless orchids as early as 1798, but Darwin thought they had to be wrong. Insects were too smart to be fooled for long. They would learn how to recognize a deceitful plant and avoid it, and the deceivers would become extinct. That turns out to be quite wrong. Over 8,000 species of orchids are believed to practice deceit. Most, like Disea nivea, mimic a food-supplying plant in their shape and odor. Others lure flies with growths that look and smell like feces. Others produce sex pheromones to lure male insects and sometimes even produce shapes that look and feel like female insects--so much so that the males try to mate with them. (More on wasp-on-orchid kinkiness here.) Orchids can in fact outfox insects, but only by continually reshaping their deceptions. Scientists suspect that the main benefit of deceit is that insects tend to fly far away after getting fooled. As a result, tend to fertilize more distant orchids, which gives the flowers a healthy supply of genetic variation.

It's fascinating to compare the story of Disea nivea to Angraeceum sequipedale. In one case, Darwin was right, and in the other he was wrong--at least in the details. His rough ideas about coevolution have developed over nearly 150 years into a huge body of knowledge about how partners shape one another over time. It just turns out that sometimes coevolution can push life in directions he couldn't imagine.

(Note: I adapted parts of the historical material in this post from my book Evolution.)

Update, Sunday 2 pm: For some reason the comments aren't going through for this post. We'll try to fix the bug today.

Update, Monday 11 am: Okay, comments are working again.

Well, Dr. Chopra has given us part two of his ruminations on evolution with a post that will make physicists cringe as much as biologists.

My favorite line: "Consciousness may exist in photons, which seem to be the carrier of all information in the universe."

Excuse me while I chat with my flashlight.

From an article on how John McCain may be positioning himself for a presidential run in The Arizona Star:

McCain told the Star that, like Bush, he believes "all points of view" should be available to students studying the origins of mankind.

"Available" is a wonderfully vague word.

Senator, Senator, a follow-up question please? Just a clarification? Do you mean that teachers just drop some pamphlets by the door that explain how we were designed by aliens? Or should that be on the final exam?

Scientists have been making some remarkable discoveries about viruses recently that may change the way we think about life. One place to start understanding what it all means is by looking at this picture.

You can't help put see a bright triangle with its three corners sitting on top of the black circles. But the triangle exists only in your mind. The illusion is known as a Kanisza triangle, and psychologists have argued that it plays on your brain's short-cuts for recognizing objects. Your brain does not bother to interpret every point of light that hits your retina in order to tell what you're looking at. Instead, it pulls out some simple features quickly and makes a hypothesis about what sorts of objects they belong to. It's fast and pretty reliable, allowing you to make quick decisions. For getting us through our ordinary lives, it's good enough. But as a guide to objective reality, it is far from perfect. What's really weird about the Kanisza trinagle is that even when you accept that it doesn't exist (cover up the circles and watch it disappear) you can still can't stop yourself from seeing it. You just have to accept that your brain's short-cuts are fooling you.

Scientists have documented lots of illusions that may expose many other mental short-cuts. And it's possible that one of them may interfere with the way we think about life. For most of the history of Western thought, natural philosophers tried to divide up living things into species and other groups on the belief that each group shared an underlying nature--an essence. Birds all have feathers, setting them off from other animals. People always give birth to people, rather than rabbits or trout. But recent psychological research suggests that essentialism is not something we come to after years of careful thought. We are essentialists from childhood. (For a nice summary of this research, see this recent article by University of Michigan psychologist Susan Gelman.) Children seem to put things into categories and come to believe that there are deep, non-obvious differences between the categories, even if they don't know what those differences are. The essence of these things is stable, children believe, and intrinsic--particularly when those things are species.

Why do we have this essence-perceiving faculty in our brains? One possibility--an adaptationist explanation--is that it helps us to predict how things will act, and allows us to come up with a reliable response. If you meet a lion, you don't need to sit down and get to know that individual lion to figure out how it will act. A lion is a lion, and you run. Of course, that particular lion might be blind or tame or a guy in a lion suit. But you're probably better off just letting the essence of lions be your guide.

Essences can act as a rough guide to organizing the world. A bird guide distinguishes different species by their unique colors and shapes. But our essentialist brains can also get us into trouble. In the 1700s naturalists could not draw clear lines between species of plants that could clearly hybridize. The discovery of the platypus in the early 1800s--an animal that nursed its young like mammals but laid eggs unlike any other mammal--posed an enormous headache. When Darwin and other scientists began arguing that humans shared a common ancestry with chimpanzees and gorillas, anatomists such as Richard Owen desperately tried to find traits in the human brain that would firmly set us apart--signs, as it were, of our unique essence. Owen failed, and today's research on the human genome helps to show what a futile effort he was making. Humans are different, just like each species is, but they are also linked to other species by common descent. They have no more of a special essence than the branches on a tree.

Which brings us to viruses. Viruses have traditionally been considered fundamentally different than "true" organisms, such as bacteria, animals, and plants. That's because all viruses that scientists studied were just simple bags of genes, made up of tiny bits of genetic material encased in protein shells. They were not truly alive, because their few genes could only be copied and turned into proteins with the help of a cell's biochemical machinery. Outside a cell, they were inert, lifeless packages drifting through the world, waiting to bump into a new host.

Last year this essence of viruses began to blur. Scientists discovered a gigantic virus capable of making 150 proteins, including enzymes for repairing DNA and for translating a gene's code into protein. Its entire genome is 1.2 million base pairs long--about twice as long as the smallest genomes of parasitic bacteria. These viruses are not rare flukes. Just a few days ago, scientists reported on how they plumbed a database of DNA gathered by Craig Venter from the Sargasso Sea and found signs that there are a lot of these giant viruses floating out in the oceans.

Today, viruses from another part of the world blurred their essence even more. Scientists reported in Nature the discovery of strange viruses from hot springs in Italy. The viruses reproduce inside microbes, and when they burst out of their host, they do not remain inert. Instead, they continue developing, growing tails made out of filament-shaped proteins that are encoded by their own genes. It's not clear from the report whether the viruses can make the proteins themselves, or if their hosts make them and then squirt them out into the surrounding water. But whichever the case, the scientists conclude that viruses "may be even more biologically sophsticated than previously recognized."

The discoverers of the "living" virus compared some of its genes to those of other organisms and argued that it has an ancient history, descending from organisms that lived four billion years ago, before the major branches of life had emerged. Some critics have argued that these viruses actually stole the genes from their hosts and incorporated them into their own genome, but the original team has rebutted them in a paper submitted to Virus Research. It is still possible that these viruses stole some of their genes from their hosts, because the evidence of viral gene theft is now overwhelming. On the other hand, viruses seem to have sometimes donated their genes to their hosts. Some researchers have even argued that many of the key components of our own cells, from DNA-copying enzymes to DNA itself--began as viruses.

So try to ignore that urge to see viruses as a separate kind from us, just as you try to ignore the triangle that isn't there. Despite what we may think, life is a wonderful blur.

The red blob in this picture is a human red blood cell, and the green blob in the middle of it is a pack of the malaria-causing parasites Plasmodium falciparum. Other species of the single-celled Plasmodium can give you malaria, but if you're looking for a real knock-down punch, P. falciparum is the parasite for you. It alone is responsible for almost all of the million-plus deaths due to malaria.

How did this scourge come to plague us? In a paper to be published this week in the Proceedings of the National Academy of Sciences, scientists have reconstructed a series of molecular events three million years ago that allowed Plasmodium falciparum to make us its host. They argue that a change in the receptors on the cells of hominids was the key. Ironically, this same change of receptors may have also allowed our ancestors to evolve big brains. Malaria may simply be the price we pay for our gray matter.

To uncover this ancient history, the researchers compared the malaria humans get to the malaria of our closeest relatives, chimpanzees. In 1917, scientists discovered Plasmodium parasites in chimpanzees that looked identical to human Plasmodium falciparum. But when some ethically challenged doctors tried to infect people with the chimpanzee parasites, the subjects didn't get sick. Likewise, chimpanzees have never been known to get sick with Plasmodium falciparum from humans. In the end, scientists recognized that chimpanzees carry a separate species of Plasmodium, known today as Plasmodium reichenowi. Studies on DNA show that Plasmodium rechnowi is the closest living relative to Plasmodium falciparum--just as chimpanzees are the closest living relatives of humans.

The authors of the new study set out to find the difference between these parasitic cousins. They focused on how each species of Plasmodium gets into red blood cells. Every Plasmodium species uses special molecular hooks on its surface to latch onto receptors on the cell, and then noses its way through the membrane to get inside. The parasite has a number of hooks, each of which is adapted to latch onto particular kinds of receptors. One of the most important groups of receptors that Plasmodium needs to latch onto are sugars known as sialic acids, which are found on all mammal cells.

These sugars play a crucial but mysterious role in human evolution. As I've written here (and here), almost all mammals carry a form of the sugar called Neu5Ac on their cells, as well as a modified version of it, known as Neu5Gc. In most mammals, this modified form, Neu5Gc is very common. In humans, it's nowhere to be found. That's because the enzyme that converts the precursor Neu5Ac into Neu5Gc doesn't work. We still carry the gene for the enzyme, but it became mutated about three million years ago and stopped working.

Since chimpanzees make Neu5Gc and we don't, the researchers hypothesized that the two Plasmodium species must use different strategies to latch onto red blood cells. To test their hypothesis, they genetically engineered cells to produce the molecular hooks used by human Plasmodium falciparum, and other cells to produce the chimp parasite hooks. The researchers then mixed the engineered cells with red blood cells from humans and chimpanzees to see how well they attached. In another set of experiments, they made human blood cells more chimpanzee-like by adding Neu5Gc sugars to them, to see if the change helped the chimpanzee parasites attack them, or if it impaired the attacks of human parasites.

Their results show that humans are uniquely vulnerable to Plasmodium falciparum because our ancestors lost the Neu5Gc sugar. Plasmodium falciparum prefers to bind to Neu5Ac, the sugar we still carry. At the same time, the sugar we lost somehow blocks Plasmodium falciparum's hooks from latching onto Neu5Ac. That's why chimpanzees don't get sick with Plasmodium falciparum, despite carrying both kinds of sugars. On the other hand, we don't get sick with chimpanzee malaria, because Plasmodium reichenowi prefers attaching to Neu5Gc, the sugar we lost.

The scientists argue that some seven million years ago the common ancestor of chimpanzees and humans carried both kinds of sugars on their cells. This ancient ape would sometimes get sick with malaria, caused by the common ancestor of today's P. rechnowi and P. falciparum. This ancient parasite preferred to latch onto Neu5Gc to get into its host's blood cells.

Hominids then branched off from other apes, walking upright and moving out of the jungle into open woodlands. They still got sick with the old malaria, because they still produced both kinds of sugars. But then, about three million years ago, our ancestors lost the ability to make Neu5Gc. Initially this was a great relief, because the malaria parasites had a much harder time gaining entry into our cells.

But this relief did not last, the scientists argue. Sometimes mutant parasites emerged that did a better job of latching onto the one sugar hominids still made, Neu5Ac. They now could get into hominid red blood cells, while other Plasmodium parasites were still making do with the other apes. Over time these parasites evolved a better ability to infect hominids. But at the same time, they surrendered the ability to infect other apes, such as chimpanzees. Thus Plasmodium falciparum was born.

This new research is yet another example of how studying evolution yields new insights into medicine. (I've blogged before about similar examples with tuberculosis and HIV.) And it may also reveal something about the downside of our unique intelligence. Our ancestors lost Neu5Gc around the time that the hominid brain began to get significantly bigger than a chimp's.

In other animals, Neu5Gc is abundant on the cells of most organs, but exceedingly rare in the brain. It is very peculiar for a gene to be silenced in the brain, which suggests that it might have some sort of harmful effect. Once a mutation knocked out the gene altogether, hominids didn't have to suffer with any Neu5Gc in the brain at all.

Perhaps Neu5Gc limited brain expansion in other mammals, but once it was gone from our ancestors, our brains exploded. Along with a big brain, however, came our very own form of malaria.

New branches on the tree of life have just turned up in Africa. Some are cuter than others.

In Madagascar, our primate family was enlarged by two adorable species of mouse lemurs. Meanwhile, other scientists made an uglier discovery in the small country of Djibouti, in the Horn of Africa. They found a surprising diversity of bacteria that cause tuberculosis. When most people think about the joys of biodiversity, they probably don't think about the hidden expanses of parasites waiting to be discovered. But in cases such as this one, they can have a fascinating story to tell--one that may prove to be important to the welfare of our own species.

Tuberculosis is, like malaria and HIV, an infectious disease so vast in its success that it's hard to fathom. Every second someone somewhere in the world gets infected with the bacteria Mycobacterium tuberculosis, and each year TB kills about 1.75 million people. Many scientists have wondered how long these bacteria have been attacking the lungs of our ancestors. Hippocrates described cases that appear to be tuberculosis, and ancient mummies show signs of the disease. For earlier chapters in the evolution of TB, scientists have begun to turn to the bacteria's DNA.

The first studies pointed to a relatively recent origin of the disease. The bacteria that scientists sampled turned out to have nearly identical DNA. If a long time had passed since the common ancestor of living strains of TB, then they would have expected to find more mutations setting the strains off from one another. Instead, they esimated that a single successful ancestor gave rise to all current strains about 20,000 to 35,000 years ago.

But French researchers have found that people in Djibouti carry strains of TB that are significantly different than anything seen before. They have many more genetic differences than have been found in human TB strains from anywhere else in the world. Yet they are more closely related to other human TB than to the Mycobacterium species that infect cattle and other animals. The scientists then turned the mutations of the Djibouti strains into a molecular clock. They estimate that the ancestor of today's human TB existed some three million years. The results have just been published in the new open access journal PLOS Pathogens.

If tuberculosis was infecting our ancestors three million years ago, it was infecting early, small-brained hominids. All of the hominids known from that time lived in Africa, and hominids would not be found outside the continent for over a million years. Our own species is believed to have evolved much later in Africa, and to have spread to Asia and Europe roughly 50,000 years ago. So it's telling that all these ancient strains are found in Africa, not far from some of the richest lodes of hominid fossils in Ethiopia. The genetic diversity of these bacteria reflects the genetic diversity of living Africans.

Some diseases are new to our species, and some are old enemies. HIV probably made the jump from chimpanzee to human in just the past century. Like other emerging diseases, its evolution is a reflection of our times. It probably is the result of roads being pushed through African rain forests for logging, allowing hunters to kill chimpanzees and sell the meat to a growing, increasingly mobile society. Other diseases appear to have gotten their start thanks to earlier opportunities. Yersinia pestis, the cause of bubonic plague, rapidly emerged a couple thousand years ago, probably taking advantage of flea-infested rats that were thriving in cramped communities. Malaria appears to have emerged a few thousand years before that, when early African farmers spend their days clearing forests and creating lots of standing water in which mosquitoes could breed, only to go to bed nearby and become easy targets for the insects.

The new study suggests that tuberculosis came long before them. But it apparently has not been with us forever--or even for five or ten million years. For some reason it appeared three million years ago, and it's intriguing think why. The new paper doesn't hazard a guess, but I'm reminded of a similar study I came across while researching my book Parasite Rex. It has to do with tapeworms.

Today tapeworms have a life cycle that take them between pigs or cows and humans, where they can grow up to 60 feet long in their intestines. In the 1940s, researchers proposed that the three tapeworm species that infect humans descend from ancestors which pioneered our guts when cattle and pigs were first domesticated some 10,000 years ago. But a close look at their DNA showed otherwise. Scientists found that the closest relatives of human tapeworms did not make relatives of cows or pigs their intermediate hosts. Instead, they lived inside East African herbivores such as antelopes, and made he lions and hyenas that kill them their final hosts. The researchers then looked at the amount of variation between the DNA from different species of tapeworms. According to the agricultural hypothesis, that variation should have pointed to a common ancestor 10,000 years ago. But the scientists concluded that this common ancestor could have lived as long as a million years ago.

The scientists proposed that tapeworms began adapting to our hominid ancestors when they began putting more meat in their diet. By scavenging or hunting on the East African savannas, our ancestors became an attractive new habitat for the tapeworms, and new species evolved that were specialized only to live inside us. Only hundreds of thousands of years later did they make cows and pigs their intermediate hosts.

Given TB's similar antiquity, I wonder if it may have made a similar leap. Many closely relatives to Mycobacterium tuberculosis live in bovids--cows and their relatives--which hominids might have encountered as they began to scavenge meat. Could a sick wildebeest have been our patient zero?

Still, the question remains: why is so much TB diversity hiding out in Djibouti, while one branch seems to have exploded about 30,000 years ago and spread around the world, such that today it makes up the vast majority of TB cases? The paper's authors hazard that this lineage spread out of Africa with the migration of humans to other parts of the world. That makes sense up to a point. The bacteria that cause ulcers, Helicobacter pylori, spread this way--so faithfully in fact that it acts as a marker for human migrations to different parts of the world. But the new TB 30,000 years ago was able to spread much more aggressively than the other strains, which apparently are still restricted to the region where they've been for millions of years. It's hard to understand what sort of social or ecological change could have created the conditions that would favor such a superior bug.

Neverthless, it may be possible to pinpoint how this new lineage evolved into such a killer by comparing it to the older strains. If scientists can identify its special weapon, they might be able to figure out how to attack it with a drug. Here, then, is one potential benefit of exploring the diveristy of parasites: you can learn how to fight the really nasty ones.

This article in the New York Times is a pretty useful overview of the political and financial support behind the Discovery Institute, the main anti-evolution think tank. It describes how the Institute has spent $3.6 million dollars to support fellowships that include scientific research in areas such as "laboratory or field research in biology, paleontology or biophysics."

So what has that investment yielded, scientifically speaking? I'm not talking about the number of appearances on cable TV news or on the op-ed page, but about scientific achievement. I'm talking about how many papers have appeared in peer-reviewed biology journals, their quality, and their usefulness to other scientists. Peer review isn't perfect--some bad papers get through, and some good papers may get rejected--but every major idea in modern biology has met the challenge.

It's pretty easy to get a sense of this by perusing two of the biggest publically available databases, PubMed (from the National Library of Medicine) and Science Direct (from the publishing giant Reed Elsevier). They don't cover the entire scientific literature, but between them, you can search thousands of journals covering everything from geochronology to genetic engineering. Look for the topics that have won people Nobel Prizes--the structure of DNA, the genes that govern animal development, and the like--and you quickly come up with hundreds or thousands of papers.

A search for "Intelligent Design" on PubMed yields 22 results--none of which were published by anyone from the Discovery Insittute. There are a few articles about the political controversy about teaching it in public schools, and some papers about constructing databases of proteins in a smart way. But nothing that actually uses intelligent design to reveal something new about nature. ScienceDirect offers the same picture. (I'm not clever enough with html to link to my search result lists, but try them yourself if you wish.)

Here's another search: "Discovery Institute" and "Seattle" (where the institute is located). One result comes up: a paper by Jonathan Wells proposing that animal cells have turbine-like structures inside them. It describes no experiments, only a hypothesis.

Perhaps the other prominent fellows of the Discovery Institute (Michael Behe, Stephen Meyer, and William Dembski) have published scientific papers that have a bearing on intelligent design, without identifying their affiliation. Aside from a couple letters to the editor, the databases yielded only one paper, in which Behe offers a simple model of gene duplication and expresses doubt that new genes could evolve by this process. Given that other scientists have published 2266 papers exploring gene duplication's role in evolution, it's safe to say that his is not a view held by most experts.

PubMed has a very nice feature that lets you get a rough gauge of how influential a paper has been. If you select "Cited in PMD" from the display option list, you get a list of papers in PudMed that have cited the paper you're looking at. The 2001 paper revealing the rough draft of the human genome has already been cited 777 times in the past four years.

Try it on the Behe and Wells papers. Total citations? Zero.

Here's one more way to put these results in perspective: compare the two papers I turned up to the work of a single evolutionary biologist. From the thousands I could choose from, I'll pick Douglas Emlen, a young biologist at the University of Montana. He studies horns on beetles as an example of how embryonic development changes during evolution (a fascinating topic I blogged on a couple months back). I visited his publication web site and counted the papers that dealt directly with evolution (leaving out the book chapters and the papers on straight physiology and such). The total so far comes to 23. Over ten times the output I found from the entire Discovery Institute staff.

Someone's not getting their money's worth.

Update: Quallitative directs my attention to the Discovery Institute's list of peer-review literature. The first item on the rather short list is a paper that has been retracted by the journal that published it, which stated that "contrary to typical editorial practices, the paper was published without review by an associate editor." Their statement also added that "there is no credible scientific evidence supporting ID [Intelligent Design] as a testable hypothesis to explain the origin of organic diversity." I don't see much more that I could add.

Update, 8/23 11pm:Steven Smith reports on his own search on another scientific database, Biosys. An independent test of my hypothesis, in true scientific spirit--and with the same results.

In today's New York Times I have an article about the quest to create a virtual organism—a sort of digital Frankenstein accurate down to every molecular detail. The creature that the scientists I write about want to reproduce is that familiar denizen of our gut, Escherichia coli.

There are two things about this enterprise I find particularly delicious. One is that this little microbe is just too complex for today's computers to handle. For now scientists are just laying the groundwork for a day that might come in 10 or 20 years when they have enough processing power to handle E. coli. Another delicious fact is that despite fifty years of intense research, scientists don't know what a lot of E. coli's genes are for. All told, this black box swallows up about a quarter of its genome.

The creationist frenzy of the past couple weeks gives these two facts special meaning. Creationists like to point out that life is very complex. They like to point out that despite years of work, scientists have yet to figure out the complete series of events by which much of that complexity evolved. This state of affairs does not represent unfinished business, according the creationists, but an outright failure. And that failure is proof that life could not have evolved. Therefore, the argument goes, life must have been directly designed by some powerful being.

To see why this argument impresses so few scientists, consider E. coli. Scientists are confident that they can explain how this microbe works with a purely mechanistic account—in other words, with the interactions of atoms, molecules, modules made of genes and proteins, and the like. It's worked reasonably well so far, allowing them to create good hypotheses how E. coli strings together proteins, builds cell walls, and so on.

But despite decades of intense research, much of E. coli remains unexplained. In their obsession with mechanistic explanations, scientists have failed to find a complete account for how E. coli works. If you buy the argument for design, you must conclude that microscopic supernatural beings dwell inside E. coli, operating it like a microbial submarine.

Of course, nobody who actually does actual research on E. coli says this. They're too busy trying to figure out how E. coli works. If you want to find examples of their work, go to scientific journals, or visit Thierry Emonet's site. If, on the other hand, you want to find people claiming that the yet-to-be-discovered is evidence of supernatural intervention, you'll have to look elsewhere. Op-ed pages are always a good place to start.

Mole rats are a pretty ugly, obscure bunch of creatures. They live underground in Africa, where they use their giant teeth to gnaw at roots. Those of you who know anything about mole rats most likely know about naked mole rats, which have evolved a remarkable society that is more insect than mammalian, complete with a queen mole rat ruling over her colony. But according to a paper in press at the Journal of Human Evolution, mole rats are important for another reason. Their evolution and our own show some striking parallels that may shed light on how our ancestors diverged from other apes.

The authors of the paper, Greg Laden of the University of Minnesota and Harvard's Richard Wrangham, believe that the rise of hominids was marked by a shift in food. Reviewing the evidence from fossils and living apes, they argue that common ancestor of humans and our three closest relatives (chimpanzees, bonobos, and gorillas) dwelled in a rain forest. If this ancient ape was anything like living chimps and gorillas, it depended mainly on fruits. When it couldn't find fruits, it turned to other so-called "fallback foods" such as soft leaves and pith.

Judging from the fossils of plants and animals found alongside early hominid bones, it seems that hominids shifted from dense rain forests to woodlands, and much later to open, arid savannas. It would have been harder to survive on the diet of a gorilla or a chimpanzee in such places. Laden and Wrangham point out that in Gabon, gorillas that live in rainforests don't venture into the surrounding savannas, despite the fact that the savannas get a lot of rain. The problem is that outside of rainforests, there just aren't enough of their fallback foods to sustain them.

So how did hominids survive? Laden and Wrangham argue that they began to rely on a new fallback food: roots, tubers, and other "underground storage units."(To me this term sounds too much as if it came from a subterranean Ikea catalog, so I'll just use the word tubers.) The idea was first proposed in 1980 by other scientists who observed that one important difference between hominids and other apes is their teeth. Chimpanzees and gorillas have shearing edges on their teeth that help them slice up leaves. Hominids had teeth that resembled those of pigs and bears, which can chew tough, fiber-rich food. Pigs dig up tubers with their snouts, bears with their claws. Fossil discoveries suggest that hominids might have used sticks or horns. But they all chewed the tubers in much the same way.

In the new paper (posted by Laden here), Laden and Wrangham explore this idea in much more detail. They point to evidence that tubers are more diverse in savannas than in rain forests, and grow at densities that can be hundreds of times higher. This makes intuitive sense when you consider that tubers are probably adaptations to dry, unpredictable climates where plants need to store away energy underground. In the stable dampness of a rain forest, there isn't much use for a tuber. Laden and Wrangham also point out that human foragers who live where lots of tubers grow take advantage of them. They prefer other food, like ripe fruits, but in tough times they dig up their meals.

Laden and Wrangham then turn from the present to the past. If their hypothesis is right, hominids must have lived in places where they might have eaten tubers. That's a tricky question to answer directly for most sites where hominid fossils have been found, because scientists haven't found enough plant fossils associated with them.

Enter the mole rats.

Mole rats love tubers, and where you find mole rats, you generally find a lot of tubers for them to gnaw on. What's more, mole rats and humans have a taste for many of the same species that produce underground storage units. Mole rats have left a long fossil record in Africa since they first appeared some 20 million years ago--not coincidentally when tuber-rich habitats may have begun to spread through Africa.

Laden and Wrangham predicted that hominids and mole rats should tend to have left fossils in the same habitats. They looked at fossil sites from six million years ago to half a million years ago in eastern and southern Africa, where hominids lived. They then picked out sites where either hominids or mole rats had been found, or both. Of the 21 sites that had mole rats, 17 also had hominids. Less than a fifth of the sites without mole-rats had hominid fossils. The pattern suggests that mole-rats and hominids both evolved to take advantage of the rich supply of tubers in African savannas. They came at the tubers from below, we from above.

Dribs and drabs of this hypothesis have trickled out over the past six years. In a 1999 paper in the journal Current Anthropology, Laden and Wrangham and their colleagues suggested that tubers were important to hominids and then became really important about 1.9 million years ago. At that time, hominids began emerging who were much taller and bigger-brained than their ancestors, and who also had smaller teeth. Laden and Wrangham argued that hominids at this time must have discovered fire, which would have allowed them to cook down tubers, liberating much of the nutrition in them. In this 2002 article Natalie Angier offers a nice summary of their thinking at the time—along with the skeptical reaction it drew from some experts. One big problem is that the oldest good evidence for fire is only a few hundred thousand years old, not almost two million.

The new paper doesn't address the skepticism about this later part of their scenario. Instead, it looks back at the first four million years of our life with tubers. Laden and Wrangham propose testing their hypothesis by looking at the trace elements and isotopes in tubers to see if the patterns are reflected in the composition of hominid fossils. I also wonder about how they got hold of the tubers. Were the earliest hominids able to fashion digging sticks, or were they merely using their hands, the way savanna baboons do today? How exactly, I wonder, did we get to be the upright mole rats?

(Update: 8/15 10 am: Thanks to Hoopman for pointing out some new findings that may show evidence of fire 1.5 million years ago. Here's a BBC article with some details. As far as I can tell, though, the results have only been presented at a conference. They haven't been published in a journal.)

It's bad enough to see basic scientific misinformation about evolution getting tossed around these days. USA Today apparently has no qualms about publishing an op-ed by a state senator from Utah (who wants to have students be taught about something called "divine design") claiming there is no empirical evidence in the fossil evidence that humans evolved from apes. I'm not sure what we're supposed to do with the twenty or so species of hominids that existed over the past six million years. Perhaps just file them away under "divine false starts."

But history takes a hit as well as science. Creationists try whenever they can to claim that Darwin was directly responsible for Hitler. The reality is that Hitler and some other like-minded thinkers in the early twentieth century had a warped view of evolution that bore little resemblance to what Darwin wrote, and even less to what biologists today understand about evolution. The fact that someone claims that a scientific theory justifies a political ideology does not support or weaken the scientific theory. It's irrelevant. Nazis also embraced Newton's theory of gravity, which they used to rain V-2 rockets on England. Does that mean Newton was a Nazi, or that his theory is therefore wrong?

Creationists are by no means the only people who are getting history wrong these days. Yesterday in Slate, Jacob Weisberg wrote an essay in which he claimed that evolution and religion are incompatible. He claims to find support for his argument in Darwin's own life.

That evolution erodes religious belief seems almost too obvious to require argument. It destroyed the faith of Darwin himself, who moved from Christianity to agnosticism as a result of his discoveries and was immediately recognized as a huge threat by his reverent contemporaries.

I get the feeling that Weisberg has yet to read either of the two excellent modern biographies of Darwin, one by Janet Browne and the other by Adrian Desmond and James Moore. I hope he does soon. Darwin's life as he actually lived it does not boil down to the sort of shorthands that people like Weisberg toss around.

Darwin wrestled with his spirituality for most of his adult life. When he boarded the Beagle at age 22 and began his voyage around the world, he was a devout Anglican and a parson in the making. As he studied the slow work of geology in South America, he began to doubt the literal truth of the Old Testament. And as he matured as a scientist on the journey, he grew skeptical of miracles. Nevertheless, Darwin still attended the weekly services held on the Beagle. On shore he sought churches whenever he could find them. While in South Africa, Darwin and FitzRoy wrote a letter together in which they praised the role of Christian missions in the Pacific. When Darwin returned to England, he was no longer a parson in the making, but he certainly was no atheist.

In the notebooks Darwin began keeping on his return, he explored every implication of evolution by natural selection, no matter how heretical. If eyes and wings could evolve without help from a designer, then why couldn't behavior? And wasn't religion just another type of behavior? All societies had some type of religion, and their similarities were often striking. Perhaps religion had evolved in our ancestors. As a definition of religion, Darwin jotted down, "Belief allied to instinct."

Yet these were little more than thought experiments, a few speculations that distracted Darwin every now and then from his main work: of discovering how evolution could produce the natural world. Darwin did experience an intense spiritual crisis during those years, but science was not the cause.

At age 39, Darwin watched his father Robert slowly die over the course of months. His father had confided his private doubts about religion to Darwin, and he wondered what those doubts would mean to Robert in the afterlife. At the time Darwin happened to be reading a book by Coleridge called Friend and Aids to Reflection, about the nature of Christianity. Nonbelievers, Coleridge declared, should be left to suffer the wrath of God.

Robert Darwin died in November, 1848. Throughout Charles's life, his father had shown him unfailing love, financial support, and practical advice. And now was Darwin supposed to believe that his father was going to be cast into eternal suffering in hell? If that were so, then many other nonbelievers, including Darwin's brother Erasmus and many of his best friends, would follow him as well. If that was the essence of Christianity, Darwin wondered why anyone would want such a cruel doctrine to be true.

Shortly after his father's death, Darwin's health turned for the worse. He vomited frequently and his bowels filled with gas. He turned to hydropathy, a Victorian medical fashion in which a patient is given cold showers, steam baths, and wrappings in wet sheets. He would be scrubbed until he looked "very like a lobster," he wrote to his wife Emma. His health improved, and his sprits rose even more when Emma discovered that she was pregnant again. In November 1850 she gave birth to their eighth child, Leonard. But within a few months death would return to Down House.

In 1849 three of the Darwin girls, Henrietta, Elizabeth, and Anne suffered bouts of scarlet fever. While Henrietta and Elizabeth recovered, nine-year old Anne remained weak. She was Darwin's favorite, always throwing her arms around his neck and kissing him. Through 1850 Anne's health still did not rebound. She would vomit sometimes, making Darwin worry that "she inherits I fear with grief, my wretched digestion." The heredity that Darwin saw shaping all of nature was now claiming his own daughter.

In the spring 1851 Anne came down with the flu, and Darwin decided to take her to Malvern, the town where he had gotten his own water-cure. He left her there with the family nurse and his doctor. But soon after, she developed a fever and Darwin rushed back to Malvern alone. Emma could not come because she was pregnant again and just a few weeks away from giving birth to a ninth child.

When Darwin arrived in Anne's room in Malvern, he collapsed on a couch. The sight of his ill daughter was awful enough, but the camphor and ammonia in the air reminded him of his nightmarish medical school days in Edinburgh, when he watched children operated on without anesthesia. For a week--Easter week, no less--he watched her fail, vomiting green fluids. He wrote agonizing letters to Emma. "Sometimes Dr. G. exclaims she will get through the struggle; then, I see, he doubts.--Oh my own it is very bitter indeed."

Anne died on April 23, 1851. "God bless her," Charles wrote to Emma. "We must be more & more to each other my dear wife."

When Darwin's father had died, he had felt a numb absence. Now, when he came back to Down House, he mourned in a different way: with a bitter, rageful, Job-like grief. "We have lost the joy of our household, and the solace of our old age," he wrote. He called Anne a "little angel," but the words gave him no comfort. He could no longer believe that Anne's soul was in heaven, that her soul had survived beyond her unjustifiable death.

It was then, 13 years after Darwin discovered natural selection, that he gave up Christianity. Many years later, when he put together an autobiographical essay for his grandchildren, he wrote, "I think that generally (and more and more as I grow older), but not always, that an agnostic would be the most correct description of my state of mind."

Darwin did not trumpet his agnosticism. Only by poring over his private autobiography and his letters have scholars been able to piece together the nature of his faith after Anne's death. Darwin wrote a letter of endorsement, for example, to an American magazine called the Index, which championed what it called "Free Religion," a humanistic spirituality in which the magazine claimed "lies the only hope of the spiritual perfection of the individual and the spiritual unity of the race."

Yet when the Index asked Darwin to write a paper for them, he declined. "I do not feel that I have thought deeply enough [about religion] to justify any publicity," he wrote to them. He knew that he was no longer a traditional Christian, but he had not sorted out his spiritual views. In an 1860 letter to Asa Gray—a Harvard botanist, the leading promoter of Darwin in America, and an evangelical Christian--he wrote, "I am inclined to look at everything as resulting from designed laws, with the details, whether good or bad, left to the working out of what we may call chance. Not that this notion at all satisfies me. I feel most deeply that the whole subject is too profound for human intellect. A dog might as well speculate on the mind of Newton."

In private Darwin complained about social Darwinism, which was being used to justify laissez-faire capitalism. In a letter to the geologist Charles Lyell, he wrote sarcastically, "I have received in a Manchester newspaper rather a good quib, showing that I have proved 'might is right' and therefore that Napoleon is right, and every cheating tradesman is also right." But Darwin decided not to write his own spiritual manifesto. He was too private a man for that.

Despite his silence, Darwin was often pestered in his later years for his thoughts on religion. "Half the fools throughout Europe write to ask me the stupidest questions," he groused. The inquiring letters not only tracked him down to Down House but reached deep into his most private anguish. To strangers, his responses were much briefer than the one he had sent to Gray. To one correspondent, he simply said that when he had written the Origin of Species, his own beliefs were as strong as a prelate's. To another, he wrote that a person could undoubtedly be "an ardent theist and an evolutionist," and pointed to Asa Gray as an example.

Yet to the end of his life, Darwin never published anything about religion. Other scientists might declare that evolution and Christianity were perfectly in harmony, and others such as Thomas Huxley might taunt bishops with agnosticism. But Darwin would not be drawn out. What he actually believed or didn't, he said, was of "no consequence to any one but myself."

Darwin and and his wife Emma rarely spoke about his faith after Anne's death, but he came to rely on her more with every passing year, both to nurse him through his illnesses and to keep his spirits up. At age 71, a few weeks before his death, he looked over the letter she had written to him just after they married. At the time she was beginning to become worried about his faith and urged him to remember what Jesus had done for him. On the bottom he wrote, "When I am dead, know that many times, I have kissed & cryed over this."

It is a disservice to Darwin, and to history, to turn his tortured, complex life into a talking point in a culture war.

(Much of this post is adapted from the last chapter of my book, Evolution.)

I'll close the week with an open letter to President Bush just released by the American Astronomical Society's president, Prof. Robert Kirschner, to express disappointment with his comments on bringing intelligent design into the classroom. Astronomers may not deal with natural selection or fossils, but as a general principle, they don't like seeing non-science and science getting confused.

Washington, DC. The American Astronomical Society is releasing the text of a letter concerning "intelligent design" and education that was sent earlier today to President George W. Bush by the President of the Society, Dr. Robert P. Kirshner.

Robert P. Kirshner
President, American Astronomical Society
Harvard College Professor and Clowes Professor of Science at Harvard University

A statement from the National Science Teachers' Association on Bush's remarks about Intelligent Design:

NSTA Disappointed About Intelligent Design Comments Made by President Bush
2005-08-03 - NSTA

NSTA strongly supports the premise that evolution is a major unifying concept in science and should be included in the K-12 education frameworks and curricula. This position is consistent with that of the National Academies, the American Association for the Advancement of Science, and many other scientific and educational organizations.

The American Geophysical Union just issued a press release in response to Bush's comments about intelligent design. It's not online at their web site yet, so I've posted it here. (Update: It's on line now.) This is not the first time that the 43,000 members of the AGU have spoken out against creationism. They protested the sale of a creationist account of the Grand Canyon in National Park Service stores, and condemned the airing of a creationist movie about cosmology at the Smithsonian Institution. But this is the first time they've taken on the President.

American Geophysical Union 2 August 2005 AGU Release No. 05-28 For Immediate Release

AGU is a scientific society, comprising 43,000 Earth and space scientists. It publishes a dozen peer reviewed journal series and holds meetings at which current research is presented to the scientific community and the public.

After a day-long road trip from Ohio, I finally had the chance to read the news that President Bush thinks that schools should discuss Intelligent Design alongside evolution, so that students can "understand what the debate is about."

As Bush himself said, this is pretty much the same attitude he had towards creationism when he was a governor. His statements back in Texas didn't actually lead to any changes in Texas schools, and I doubt that these new remarks will have much direct effect, either. But, like Chris Mooney, I'm a journalist, and like him I would have loved to have been in the crowd of reporters when Bush made these remarks.

Mooney would have asked Bush how he squares his comments with those of his own science advisor, John Marburger, who dismisses Intelligent Design out of hand. I would follow up on his question by expanding it to a much bigger scale.

Mr. President, I would ask, how do you reconcile your statement that Intelligent Design should be taught alongside evolution with the fact that your administration, like both Republican and Democratic administrations before it, has supported research in evolution by our country's leading scientists, while failing to support a single study that is explicitly based on Intelligent Design? The National Institutes of Health, the National Science Foundation, and even the Department of Energy have all decided that evolution is a cornerstone to advances in our understanding of diseases, the environment, and even biotechnology. They have found no such value in Intelligent Design. Are they wrong? Can you tell us why?

For plenty of other comments, you can follow the links at Pharyngula

Update 8/2 7:45 pm: I might also ask the President to respond to 43,000 scientists who think he's putting schoolchildren at risk.

Update 8/3 5:30 pm: Or 55,000 science teachers who are shocked and disappointed by his remarks.

Update 8/6 9:30 am: Or the nation's astronomers, who think his remarks are bad for all science.

I've been fascinated by this picture since I first saw it over the weekend. It's a hint of how we may be visualizing life in years to come.

As Darwin was trying to figure out how new species could evolve from old species, he began to think of evolution as a tree. He scribbled some simple branches in a notebook, and then published a more elaborate one in The Origin of Species. Darwin didn't actually put any animals or plants on the branches of these trees; he was just thinking about the process itself. Today, though, evolutionary trees are a common sight in scientific journals, whether scientists are reconstructing the origin of a new strain of HIV or are trying to figure out how animals evolved from single-celled ancestors.

But scientists have also realized that drawing trees is harder than it once seemed. Evolution, at its heart, is about changes to DNA. For some organisms, like ourselves, DNA changes almost entirely as the result of mutations when parents bequeath their genes to their offspring. But it is possible for genes from one organism to hop to another. This happens most often in microbes. A bacterium may jam a needle into another bacterium and inject some genes. In other cases, viruses may pick up the genes of one host and bring them to a new host. Once a gene makes this jump, it may then get carried down through normal heredity to the receiver's descendants, spreading into new species that evolve from it.

Scientists are trying to figure out how important this kind of species hopping has been over the history of life. In a sense, scientists are asking what is the shape of the tree of life? Is it for the most part an ordinary tree as Darwin pictured it, with a few vines representing jumping genes? Or are the vines so dense that they obscure parts of the tree altogether? This debate is not a huge issue when it comes to the evolution of animals (although viruses have shaped our genome). Most of the evidence for these vines comes from bacteria and other microbes, which are very promiscuous with their genes. Most of the diversity of life is microbial, and microbes were the only game in town for the first couple billions years of the history of life. So the stakes of this debate are big.

This picture is a splendid representation of this debate. Scientists at the European Bioinformatics Institute created it by comparing 184 microbes. The scientists first identified genes that the microbes all inherited from a common ancestor that they then passed down in conventional parent-to-offspring fashion. By comparing their different sequences, the scientists were able to draw a conventional tree of the sort Darwin had in mind. Next, they scanned the genomes of these microbes for jumping genes. They drew the jumpers as vines from one branch to the next. They then produced this three-dimensional picture.

As you can see, the branches rise from a common ancestor, but they are enmeshed in vines. What's particularly fascinating about it is the way in which the vines connect the branches. It is not a random mesh. Instead, a few species are like hubs, with spokes radiating out to the other species. This is the same pattern that turns up in many networks in life, from the genes that interact in a cell to the nodes of the Internet. These hubs can bring a vast number of nodes into close contact. It's why you can play Six Degrees of Kevin Bacon. In the microbial world, this network allows genes to move quickly through the tree of life, whether those genes provide resistance to antibiotics or allow microbes to cope with some other change in the environment. The Kevin Bacons of the microbial world, at least in the current study, seem to be species that live in habitats where they may come in intimate contact with other species, such as in plant roots. They then act as gene banks from which other species can make withdrawals.

Of course, 184 species of microbes represent a vanishingly small sample of the diversity of life on Earth. It remains to be seen if the Kevin-Bacon structure survives as more branches and vines get added to this picture. But this is an important step forward in how we envision life. Perhaps in the future, this tangled tree will take its place alongside Darwin's notebook scribbles.

Science Magazine is celebrating its 125th anniversary with 125 big questions that scientists will face in the next 25 years. You can read them all for free here. For the 25 biggest questions, the editors commissioned short essays. I addressed the minor matter of how and where life began.

Fortunately, I get to ask the question. I don't have to provide the final answer. A science writer's prerogative.

This week a few more tantalizing clues about the origin of language popped up.

I blogged here and here about a fierce debate over the evolution of language. No other species communicates quite the way humans do, with a system of sounds, words, and grammar that allows us to convey an infinite number of ideas. While particular languages are the products of different cultures, the basic capacity for language appears to be built into our species. Some scientists argue that language is primarily the product of natural selection working within the hominid lineage over the past few million years. Others suggest (argue might be too strong a word) that a lot of the components of language may have already been in place before our ancestors parted evolutionary ways with other apes. That would leave natural selection with a relatively small role in giving rise to human language.

Debates in evolutionary biology can be fierce and sometimes even ugly, and as a result they can give the misleading impression that the two sides are as different as black and white. Usually, however, the debate is over how much natural selection was responsible for shaping a feature in its current form and function. Take the evolution of bird feathers. Birds use them for flight, and they are exquisitely adapted for flight in their subtlest details. But fossils suggest that dinosaurs had feathers long before birds flew. So natural selection for flight did not produce feathers. As the ancestors of today's birds started flying, however, natural selection probably then sculpted their feathers for better performance in the air.

In the case of the language debate, both sides agree that hominids inherited a set of capacities that may now play a role in language. Both sides agree that at least some natural selection helped shaped those capacities. The question is how far to either side the balance actually was. The best way to set that balance is to find more clues about the origin of language.

The first clue comes from squeaky mice.

In 2001 scientists identified a gene involved in spoken language. They found it by studying a Pakistani family in which half the members suffered from a disorder that interfered with their ability to understand grammar and to speak. The scientists tracked the disorder back to a single mutation to a single gene, which is now known as FOXP2.

FOXP2 belongs to a family of genes found in animals and fungi. They all produce proteins that regulate other genes, giving them a powerful role in the development of the body. FOXP2 in particular exists in other mammals, in slightly different forms. In mice, for example, the part of the gene that actually encodes a protein is 93.5% identical to human FOXP2.

The following year another group of scientists compared the human version of FOXP2 to the sequence in our close primate relatives. They found that chimpanzees have a version of the gene that's hardly different from the gene in mice. But in our own lineage, FOXP2 underwent some fierce natural selection. By comparing the minor differences in FOXP2 carried by different people, the scientists were able to estimate when that natural selection took place--roughly 100,000 years ago. That's about the time when archaeological evidence suggests that humans began using language. (For a good review of all this work, go here.)

What exactly was FOXP2's role in the evolution of language? A group of scientists decided to see what sort of role it played in other animals. They genetically engineered mice lacking FOXP2 (some had one copy, others had none). Then they watched the mice develop. As the scientists reported this week, the mice experienced many changes, but the most tantalizing one reported in a paper this week was in their squeaks. Mice communicate with one another a great deal with ultrasonic sounds, and their squeaks can convey a lot of information. They are particularly important for pups, so that they can get help from their mothers. Pups missing FOXP2 had serious trouble squeaking for Mom when the scientists removed them from their nests. The trouble did not lie anywhere in their vocal tract, which developed normally. The scientists found instead that the neurons in a region of the brain at the back of the head known as the cerebellum hadn't developed properly. The cerebellum is known to play a vital role in motor control, so perhaps that mice couldn't manipulate their throats properly.

Before this study, scientists already knew that FOXP2 was important to the development of other animals, but now the evidence suggests that the gene was already playing a role in communication in the common ancestor of mice and humans, perhaps 80 million years ago. Given that the FOXP2 gene in chimpanzees and mice is barely different, it seems to have evolved little in our ancestry from 80 million years ago to 6 million years ago. That's interesting when you consider that primates have some pretty elaborate communication systems, and that a clever chimpanzee can be taught a simple language by humans. Perhaps FOXP2 was continuing to play a role in the brain's control of the voice anatomy, while other genes were evolving to handle other aspects of communication. And if FOXP2 in fact only underwent significant evolution in our lineage after we split from other apes, the new research may give a clue as to what happened during the evolution. People with mutations to FOXP2 have trouble controlling their mouths, and they had trouble with grammar. Perhaps it took on this second role in the past 100,000 years.

As I blogged here, scientists have looked for more clues to the function of FOXP2 with brain scans. They compared activity in the brains of people with mutations to FOXP2 to people with normal versions of the gene as both sets of people did different language tasks, such as thinking of verbs that go with nouns. The scientists found that a change to FOXP2 changes the way the brain handles language. Specifically, in people with mutant copies of the gene, a language processing area of the brain called Broca's area is far less active than in people with normal FOXP2.

Broca's area has a long history in neuroscience. In 1861 the French physician Pierre Broca treated a man who had suffered a stroke that robbed him of his ability to say anything except the word "Tan." (He said it so much that he was nicknamed Tan.) Despite this devastating blow to his faculty of language, he could still understand the speech of other people. After Tan's death, Broca autopsied his brain to find exactly what part of the brain had been damaged. It turned out that the stroke had destroyed part of Tan's left frontal lobe. Broca looked at other patients with the same condition (known as aphasia), and found that they too suffered damage in the same area--what came to be known as Broca's area.

Scientists are still trying to figure out what Broca's area actually does in language. It's possible that it does several things at once, or that it's actually a collection of smaller regions that have different jobs. While Broca's area may help us control our mouths, that's not its only role. In the recent scanning experiment I mentioned, it became active even when people just thought about words.

The second clue this week comes from Broca's area—or at least the corresponding part of a monkey's brain.

Monkey brains and human brains are similar enough that scientists can find some of the regions in one species in the other, albeit in a different size and shape. There's been a lot of debate, however, about whether a counterpart to Broca's area exists in monkeys. If it didn't, that would suggest that it must have emerged in our own lineage after the split with the ancestors of living monkeys.

This week in Nature, scientists report that monkeys do have Broca's area. They show that the neurons in a patch on the left side of a monkey's brain are organized in the same ways as Broca's area. The patch also borders areas that have already been identified as being the same areas that border Broca's area. The scientists then put microelectrodes in the brain region and ran small currents through it to see what would happen. The monkeys moved their jaws and tongues. So Broca's area was already controlling the mouth 30 million years ago. At some point later, apparently, it became more adapted for speech in our lineage. Exactly how FOXP2 got involved in Broca's area remains a mystery.

These two clues don't show exactly where to set the balance between "pre-adaptation" and natural selection when it comes to language. But they do help reveal the building blocks that were put to use at some point.

Last year I went to a fascinating symposium in honor of the great evolutionary biologist George Williams. The March issue of the Quarterly Review of Biology ran a series of papers written by the speakers at the meeting that offered much more detail on how Williams had influenced them in their various fields. Randolph Nesse of the University of Michigan gave one of the most interesting talks at the meeting on maladaptation and what it means to human medicine. You can download the pdf from his web site.

To whet your appetite, here's a nice passage on the eye:

"It works well when it works, but often it does not. Nearly a third of us have hereditary nearsightedness, and almost no one over 55 can read a phone book unassisted (except for those who have been nearsighted for decades!). The lovely mechanism that regulates intraocular pressure often fails, causing glaucoma. Then there is the blind spot, a manifestation of the abject design failure of nerves and vessels that penetrate the eyeball in a bundle and spread out along the interior surface instead of penetrating from the outside as in the betterdesigned cephalopod eye. Octopi not only have a full field of vision, but they need not worry about retinal detachment. They also need neither the tiny jiggle of nystagmus that minimizes the shadows cast by vessels and nerves on the vertebrate retina nor the brain processing mechanisms that extract the visual signal from the nystagmus noise. In short, the vertebrate eye is a masterpiece not of design, but of jury-rigged compensations for a fundamentally defective architecture."

In the comments, Doug gets exasperated with some recent posts of mine:

“Isn't it amazing how everything seems to provide evidence for evolution? The brain shrinks in some form of pygmy homo erectus. Thats evolution! Ancient genes survive millions of years unchanged. That's evolution?! Women have orgasms. That's evolution! Although not all women have orgasms and they still manage to reproduce hmm luckily with the right spin...That's evolution! We live in a civil society with people working for cooperative goals. That's evolution! Unfortunately some people murder and rape. Just an unfortunate side-effect, but that's evolution.

“Not only is everything evidence for evolution but evolution explains everything! No its not circular reasoning its Evolution! Thank goodness we don't need to resort to God to explain the world around. Now we have Evolution! Its the all-encompassing answer to the ultimate question (I always thought it was 42). The evolutionist has reached the omniscient nirvana. maybe we should start meeting at the biology lab on Sunday mornings. We can sing some Evolution Hymns. Do they exist? Don't worry they'll evolve. I'll just start selectively pressing some keys on the organ and type a few letters while blindfolded. Okay I'm getting a little carried away...chalk it up to evolution.” [sic]

I find that in situations like this, it helps to step back for a moment from evolution and look at the other major scientific theories of the past couple centuries that explain a lot about the natural world. You could translate Doug's complaints about evolution into complaints about any of them.

Take the theory of plate tectonics. According to this theory, the Earth is covered in plates of crust. Each plate grows along one margin with molten rock that rises from the Earth's interior. The margin on the other side of the plate is cold and sinks down into the interior, where it is remelted and mixed up with the rock down there. Continents ride on top of these plates. In some cases they crash into each other, such as India and Asia, forming mountains. In other cases, a new rift splits a plate apart, pushing continents away, as with Africa and South America.

From the 1920s to 1960s, geologists put together this theory as a way to explain patterns on the Earth. They couldn't actually see the continents crash into each other like bumper cars, because the process takes millions of years. Instead, they had to develop hypotheses that they could then test by looking at the Earth. For example, they calculated the age of rocks around mid-ocean ridges. The rocks closer to the ridges were younger than the ones further away. Years of studies both in the field and in the lab have strengthened the theory, but they've also led scientists to expand it from its original form. The original theory didn't account for what was driving hot rock up from the interior in the first place, for example. Yet new ideas for these sorts of things do not invalidate the realization that the continents move.

Now imagine a blog about plate tectonics (I wish there was one). The blog is dedicated to new research into how all the dizzying variety of landscapes on the planet, from jagged cliffs to undersea volcanoes, are produced by the Earth's geological engine. It could even have a few posts about how plate tectonics helps explain some things you might never expect geology to explain, such as why it is that some animals in Africa and South America are surprisingly similar. Answer: their common ancestors lived at a time when the two continents were still joined together.

Imagine the sort of exasperated comments such a blog would get:

"Isn't it amazing how everything seems to provide evidence for plate tectonics? Continents split apart. That's plate tectonics! Continents crash into each other. That's plate tectonics?! Plates sink under other plates. That's plate tectonics. Although some plates actually slide past each other. That's plate tectonics. Not only is everything evidence for plate tectonics, but plate tectonics explains everything! No it's not circular reasoning, it's plate tectonics! Thank goodness we don't need to resort to God to explain the world. Now we have plate tectonics!"

Any theory that would explain the Earth's landscape has to be able to account for a huge variety of features. The same goes for any theory that would explain the Earth's biological diversity. Just consider fish. There are fish with eyes and fish without. Most fish only swim, but some fish can fly and some can crawl on dry land. A theory that could only shed light on one kind of fish wouldn't be much of a theory at all.

The theory of evolution explains this variety, but not in an arbitrary way. Fish descend from a common ancestor, and along the way they have been modified, primarily through natural selection, into different forms. Flying fish do not have wings made out of balsa wood. Their wings are actually modified fins. The fins that some fish use to crawl on land are also clearly modified from the fins other fish use to swim. Fish without eyes still retain the genes required to form eyes, but they have been modified so that the eyes never fully develop. If these fish really did evolve from a common ancestor, you'd expect that their DNA would reflect this common kinship. And it does. If these fish really did evolve from a common ancestor, you'd expect that the fossil record would be consistent with their descent. And it is.

As a result, the specific examples that Doug brings up are not circular, but rather are particular cases of well-studied patterns in evolution.

Dwarfing is not an idea that someone came up with when Homo floresiensis was discovered. It's been documented in many animals. Is there a compelling explanation for how full-sized elephants come to islands and then become the size of cows other than evolution? Let's hear it.

The genes Doug refers to are the ones found in jellyfish and humans. As animals, we descend from a common ancestor. We have lots of genes in common with jellyfish—genes for building cells, proteins, and DNA, for example. Now it turns out that some body-building genes are also conserved in humans and jellyfish. But these genes are not carbon copies of one another. They have been modified in each lineage, just as you'd expect if life did indeed evolve.

Doug's example of female orgasms raises another important point: an overarching theory about the history of life or the Earth does not automatically give you all the answers about that history. How did the Andes Mountains form? If a geologist simply says, plate tectonics, that's not a very satisfying answer. Yes, plate tectonics were involved, but how? It turns out that the best explanation geologists have is a staggeringly complex interplay of continental collision, flowing rivers, and climate change. But the issue is still very much in debate. Orgasms are also an open question, as are the precise evolutionary origins of many things in nature. Natural selection may well turn out not to have much to do with human female orgasms. We'll see.

If a scientific theory can explain an aspect of the natural world, withstand scrutiny, and lead to important new insights into how the world works, we really shouldn't hold its success against it. No one's asking for evolution hymns—certainly no more than they're asking for gravity hymns or hymns to the periodic table of the elements.

Back in 1986 a biologist named Cindy Lee Van Doverwas poking around the innards of shrimp from the bottom of the sea. They came from a hydrothermal vent in the Atlantic, where boiling, mineral-rich water came spewing up from cracks in the Earth’s crust and supported rich ecosystems of tube-worms, microbes, crabs, and other creatures. The animals that lived around these vents were generally blind, which wasn’t surprising considering that no sunlight could reach them. But Van Dover noticed that they had two flaps of tissue running along their backs that connected to nerves. Closer inspection revealed that the tissue was actually made of light-sensitive pigments and photoreceptors. What, Van Dover wondered, could these shrimp possibly be looking at. Dives to mid-ocean ridges later revealed that the vents produce a faint light of their own.

In 1996 I wrote a story for Discover about Van Dover’s obsession with deep-ocean light. At the time she was fascinated by the possibility that vents might make enough light to support photosynthesis. The sunlight that reaches the Earth’s surface is a million times brighter than vent light, but scientists have found microbes 240 feet down in the Black Sea that can survive on an equally scanty supply of photons. But at the time it was just speculation.

It is very cool to see that nine years later Van Dover hasn’t lost the obsession. In a paper just published in the Proceedings of the National Academy of Sciences, she and her colleagues report their discovery of photosynthetic bacteria living around deep-sea vents. On a cruise to the East Pacific Rise, the scientists bottled vent water and then took it to a lab to culture the microbes they had trapped. One species was able to grow only in the presence of light, which it absorbed with photosynthetic pigments. The researchers doubt that the microbes drifted into the bottles from somewhere else because they seem well-adapted to the vents. They feed on sulfur compounds that are spewed up through the vents. The water around the vents is poor in oxygen thanks to chemical reactions there, and the bacteria thrive in the absense of oxygen. The nearest place where the bacteria might enjoy these features is thousands of miles away from the vents.

Over at Cosmic Log, Alan Boyle discusses what this discovery means for the search for life elsewhere in the universe. Short answer: photosynthetic organisms might be dwelling in the dark on other planets. I found myself thinking about another implication of the discovery, which I discussed in my 1996 article. Photosynthetic life may have existed on Earth 3.7 billion years ago, and scientists would like to know how the necessary chemistry for harnessing sunlight first evolved. Van Dover and her colleagues suggested that it might have gotten its start around hydrothermal vents. It could have evolved from a means for simply detecting light. Like shrimp, microbes don’t want to get too close to the water coming directly out of a vent because they’ll get fried. Over time, these bacteria might have evolved the ability to harness the energy of the light as well. Later, some of these deep-sea photosynthesizers might have been carried to shallower vents, where they might also be able to catch light from the sun. From these migrants came the sunlight-harnessing molecules that allow bacteria to consume trillions of tons of carbon. Some algae acquired this machinery as well, probably by eating photosynthetic bacteria, and they in turn gave rise to land plants. In other words, our forests and lawns got their start at the bottom of the sea.

These newly discovered bacteria don’t clinch this argument by any means. They are not living fossils unchanged for four billion years. But they at least show that a key part of this evolutionary scenario is plausible: that photosynthetic organisms can survive around deep-sea vents. That’s certainly an idea that nobody thought of before Van Dover began poking around in dead shrimp.

I’ve got an article in today’s New York Times about jellyfish and their kin—known as cnidarians. Cnidarians look pretty simple, which helped earn them a reputation as simple and primitive compared to vertebrates like us, as well as insects, squid, and other creatures with heads and tails, eyes, and so on (known as bilaterians). But it turns out that a lot of the genes that map our complex anatomy are lurking in cnidarians, too. Scientists are now pondering what all that genetic complexity does for the cnidarians. They’re also using these findings to get a better idea of how the major groups of animals evolved between 600 and 500 million years ago.

For those interested some of the gorey details, check out PZ Myers’s take. Be sure to follow the links to earlier comments on some of the key papers on this research, plus diagrams.

In addition, curious readers can check out:

The timing of the evolution of cnidarians and bilaterians (full text)

An ode to the starlet sea anemone, which has revealed a lot of the secrets of the cnidarians (abstract only)

The evolution of diploblasty (development from two embryonic layers)

Update, 4:20 pm: PZ Myers link fixed (and spelling corrected!).

It’s strange enough that beetles grow horns. But it’s especially strange that beetles grow so many kinds of horns. This picture, which was published in the latest issue of the journal Evolution, shows a tiny sampling of this diversity. The species shown here all belong to the genus Onthophagus, a group of dung beetles. The colors in this picture, which are false, show which parts of the beetle body the horns grow from. Blue horns grow from the back of the head, red from the middle of the head, and purple from the front of the head. Green horns grow from the center of the body plate directly behind the head (the pronotum), and orange horns grow from the side of the pronotum. These beetles can grow horns big and small, single or multiple, shaped like stags or like rhinos. And, as these colors show, the beetles can take very different developmental paths to get to their finished product. The biologist JBS Haldane was supposedly asked once if he could say anything about God from his study of nature. Haldane replied He must have an inordinate fondness for beetles. Add to that a fondness for putting horns on those beetles.

A century before Haldane, Charles Darwin was fascinated by the horns of these beetles. He proposed that they were produced through sexual selection. Natural selection was based on how traits helped an organism survive and have offspring—staying warm in winter, fighting off diseases, and so on. Sexual selection was based on the struggle to have sex. If females preferred to mate with males with certain traits (big tails in peacocks, for example), the males would gradually evolve more and more elaborate versions of that trait. Males might also fight with other males to get access to females, and here too their struggle could lead to baroque anatomy—such as beetle horns.

Modern evolutionary biologists have followed up on Darwin’s suggestion, and have made a close study of beetle horns. There are thousands upon thousands of species with horns to compare, and scientists can observe how the horns develop and are used by the males. A lot of fascinating work has been published on beetle horns, such the work I described in this post. The picture I’ve shown here comes from a paper that represents a big step forward in understanding this explosion of diversity. Douglas Emlen of the University of Montana and his colleagues have, for the first time, reconstructed some of the evolutionary history that produced this embarrassment of horns. (You can download the paper for free here on Emlen’s web site.)

Emlen and his colleagues focused their attention on Onthophagus dung beetles. These beetles, which are found all over the world, search out dung and then dig a tunnel underneath it. The female beetles then make a ball of the dung and lay eggs in it. The male beetles will guard the opening of these tunnels and fight off any males that try to get in and mate with the female inside. It’s here the horns come in handy, helping a guarding male make it impossible for other males to get past them.

The scientists extracted DNA from 48 different species of Onthophagus and used the sequence to figure out their evolutionary relationships. They then reconstructed the changes that evolved in the horns as new species arose. And finally, the researchers looked at the natural history of the animals—where they lived, how they lived, and the like.

It turns out that beetle horns have changed a lot. Judging from the species that sit on the oldest branches of the tree, the scientists concluded that the common ancestor of these 48 beetle species had a single horn growing from the base of the head (the second from the top on the left hand side of the photo may bear a resemblance). As new species arose, they tended to grow bigger horns, and they also tended to grow horns from new parts of their bodies. On the other hand, sometimes a lineage with elaborate horns gave rise to species with much smaller ones. Sometimes one horn became two which became one. This chart shows the tortuous paths that evolution has taken in these beetles. (The thickness of the arrows shows how often these transformations took place in different lineages.) Given that the researchers analyzed only 48 out of the 2000 Onthophagus species, the true scale of change is probably far greater.

Emlen and his collagues argue that sexual selection has driven the horns of these beetles to outrageous lengths. If you’re a male dung beetle and you want pry another male out of his tunnel, it helps to have a longer horn. If you’re that male in the tunnel, your own chances of victory depend on the horn too. So it’s the males with bigger horns that are most likely to win. And yet, as this beetle flow chart shows, these insects have lost their weaponry in some lineages. What is the countervailing force in beetle evolution?

Horns, the scientists point out, are expensive. It takes a lot of energy and the dedication of large swaths of a beetle’s body to grow horns. When you’re talking about horns that can get longer than a beetle’s entire body, the costs can be huge. In fact, growing bigger horns means that beetles have to reduce the size of other organs. Experiments have shown that the growth of horns can reduce the size of beetle eyes by 30%.

The researchers proposed that growing horns would force a trade-off with other important parts of the body, such as eyes and antennae. And the beetle tree supports their proposal. It is harder for beetles to detect the odor of dung with their antennae in a pasture than in a forest, because the odor plumes last longer in the woods. Four out of the five gains of new horns took place in forests—perhaps because beetles could afford to grow smaller antennae in a place where smelling wasn’t so hard. On the flip side, in seven of the nine cases in which horns were lost, the beetles became nocturnal. Beetles that fly at night need larger eyes, and so they can’t afford to shunt resources to big horns any more. The pressure to evolve bigger horns still exists in these lineages, but it’s been offset by other demands.

Emlen's study is a nice reminder that we don't have to stand back, slack-jawed, at nature's diversity. When you look at a line-up of beetle horns like the one at the beginning of this post, they can seem like an impenetrable mystery. But understanding of how these beetles live, and how they evolved from a common ancestor, makes them less mysterious. But no less marvelous.

Today in Science scientists reported a potentially big advance in creating embryos that can be used for stem cell transplants. Briefly put, they figured out how to take skin cells from patients, inject them into donated eggs emptied of their own DNA, and nurture them along until they had divided into a few cells. The cells were able to develop into a wide range of cell types, their chromosomes were normal, and they were so similar to the cells of the indvidual patients that they would not be rejected as foreign tissue. The research stopped there, but the dream behind this work is to heal your failing liver or heart or dopamine-producing neurons by clipping off a little skin and farm new cells that could regenerate those organs.

This research was designed in part to overcome a problem with stem cells that is part of the evolutionary baggage we carry--a problem I blogged about in January. Traditionally embyros have been nurtured by "feeder cells" from mice and calf serum. This turned out to cause make these embryos--and any stem cells derived from them--useless due to contamination. Roughly two million years ago, our ancestors lost a gene that produced a sugar on the surface our cells. Other mammals still produce it. The earliest hominids probably produced it too. But new species of hominids that emerged after two million years ago, such as our own and Neanderthals, didn't have it.

It turns out that if you feed an embryo with cells or serum from other mammals, they will absorb the sugar and stick it on their surface. To the human immune system, they look foreign. In other words, human evolution can shed light on current stem cell research. The scientists who did the new research figured out how to avoid rejection by coming up with a way to nurture the embryos with human feeder cells, so that they could avoid sticking sugars on the stem cells that our ancestors lost long ago.

Reading about this advance, I felt a grim sense of irony. As I wrote in my original post, President Bush stopped federal funding for research on stem cells using new lines derived from embryos, despite the fact that most of the already existing lines were contaminated by this lost sugar. American scientists have been making some progress with stem cells with private money and state initiatives, but guess where scientists finally figured out how to solve this evolutionary problem with cell sugars? South Korea.

Reading about this research, I was also reminded of an article I read last week during the Kansas "trial" over evolution and creationism.

Leonard Krishtalka, the director of the Kansas University Natural History Museum, was quoted pointing out how Kansas is raising $500 million to foster a bioscience and biotech industry in the state. It was ironic, he said, that the state's board of education was simulataneously "trying to remove and water down the basic fundamental concept of evolution that underlies all of biology."

Case in point: try to imagine a stem cell therapy company deciding where to set up shop. I doubt they'd be excited about a state that doesn't make sure their high school students understood mutations, natural selection, the origin of species, the fossil record, and all the other elements of evolutionary biology--that thinks it's fine just to claim that the broken sugar gene in our genome was just stuck there for reasons unknown by some mysterious designer.

Judging from fossils and studies on DNA, the common ancestor of humans, chimpanzees, and bonobos lived roughly six million years ago. Hominids inherited the genome of that ancestor, and over time it evolved into the human genome. A major force driving that change was natural selection: a mutant gene that allowed hominids to produce more descendants than other versions of the gene became more common over time. Now that scientists can compare the genomes of humans, chimpanzees, mice, and other animals, they can pinpoint some of the genes that underwent particularly strong natural selection since the dawn of hominids. You might think that at the top of the list the scientists would put genes involved in the things that set us apart most obviously from other animals, such as our oversized brains or our upright posture. But according to the latest scan of some 13,000 human genes, that's not the case. Natural selection has been focused on other things--less obvious ones, but no less important. While the results of this scan are all fascinating, one stands out in particular. The authors of the study argue that much of our evolution is the result of a war we are waging against our own cells.

It's possible to reconstruct the history of natural selection thanks to a quirk in DNA. Genes carry the code for making proteins, but it's possible to change the code without changing the resulting protein. Consider for example how cells stick new amino acids at the end of growing proteins. The nucleotides in a gene can't have a one-to-one correspondence to amino acids, since there are only four nucleotides in DNA and twenty amino acids. Instead, the cell reads three nucleotides at a time from a gene, and then chooses its amino acid. The triplet CUU makes the amino acid leucine, for example. But so does CUC and CUA. In many cases, the last nucleotide in a triplet is irrelevant.The most intriguing result of this study is that we appear to be in an intense war with our own cells.

If a hominid's genes mutated such that CUC became CUA, the mutation would have no effect for good or bad on that hominid, because the mutation didn't change its proteins. Scientists have found that mutations to "non-coding" DNA can slowly spread through an entire species thanks merely to chance. If you compare a particular gene from a human and a chimpanzee and a gorilla, you'll see that each species has picked up some silent mutations since it split off from the common ancestor of all three species.

But mutations that actually change a protein's structure are a different kettle of fish. Many of them turn out to be outright disasters, leading to diseases, spontaneous abortions, and so on. These mutations tend to be weeded out by natural selection. On the other hand, mutations that change proteins in an adaptive way can spread quickly. And if a protein is under intense natural selection, a whole series of mutations to coding DNA may build up in its gene.

One sign that a gene has undergone intense natural selection in the past is the ratio of mutations to its coding DNA to mutations to its non-coding DNA. If the coding mutations significantly outnumber the non-coding ones, it's a safe bet that this ratio is the result of intense natural selection. There are other methods for detecting natural selection, but what I've described here is the basic idea behind the new PLOS Biology paper. Expanding on an earlier scan, the researchers looked for genes that showed signs of significant natural selection by comparing their sequences in humans and chimps. They then sorted these genes according to which organs they are active in the most, and made a "Top-50" list of the genes that have undergone the most intense natural selection.

The human brain, remarkably enough, shows no sign of harboring a lot of fast-evolving genes compared to other organs. "In fact," the authors write, "genes expressed in the brain seem to be among the most conserved genes with the least evidence for positive selection." Instead, they suggest, our unparalleled brains may have evolved through adaptive changes in relatively few genes, or perhaps by borrowing existing genes that were active elsewhere in the body (I've blogged about this gene-borrowing here).

So where did all the intense selection take place? Some of it turns up in the immune system, which must battle a rapidly evolving army of parasites. Some of it turns up in the nose, possibly in order to sniff out dangerous foods or possibly to recognize suitable mates. Some of it seems to be involved in how sperm and egg recognize one another. But the most fascinating set of fast-evolving genes do something else altogether: they control the way cells kill themselves.

Suicide is essential for a healthy body. Cells kill themselves for many good reasons--to protect other cells if they are infected with a dangerous pathogen, for example, or to stop the growth of an organ once it reaches the right size. Our hands would look like webbed duck feet if the cells between our fingers didn't commit suicide.

Sperm turn out to be a particularly suicidal bunch. Three-quarters of potential sperm cells kill themselves. Some researchers have suggested that they are so prone to suicide because their population needs to be kept in balance with the other cells in the testes that nourish them. The death of the individual sperm benefits the entire population--and thus the man who carries them.

On an evolutionary level, this creates a conflict between sperm and man. If one of the cells should mutate in such a way that it could escape suicide, it could reproduce madly while other sperm cells dutifully destroyed themselves. These mutant sperm would then be more likely to reach an egg, and as a result the mutant suicide gene would become more common.

While this kind of mutation may favor an individual sperm, it may do harm to its owner. His overall sperm production might suffer as a result of this mutiny down below, for example. It might even increase his risk of cancer. After all, one of the hallmarks of cancer is the mutation of suicide genes, allowing cancer cells to grow rapidly into tumors. Once a sperm fertilized an egg, its suicide-escaping genes would wind up in every cell of the resulting person, raising their chance of turning cancerous. (See this post for more on the intersection of evolution and cancer.)

The authors of the study point out that many of the genes that end up near the top of their list have long been known to be involved in cancer. Perhaps, they suggest, many cases of cancer are the result of this pressure on sperm to escape suicide. And if their hypothesis is right, then you'd expect that a mutation that can stop these renegade sperm from wreaking havoc might be favored by natural selection. There are a number of genes that are crucial for suppressing tumors, and--as predicted--they are also among the fastest-evolving genes. In fact, some of these fast-evolving tumor suppressing genes are only active in the testes, where they may be keeping sperm in check.

This sort of two-level evolution may seem bizarre, but biologists are documenting a growing number of cases of it. It was particularly important, for example, in the evolution of multicellular animals from singe-celled protists some 700 million years ago. But it's hardly ancient history, this new study suggests. Every time cancer strikes, it makes its presence known.

Update, 7pm: PZ Meyers offers a detailed tour of the Top 50.

On Thursday I predicted that pundits would make the rediscovery of the Ivory-billed woodpecker an opportunity to criticise predictions that humans are causing mass extinctions--while conveniently ignoring evidence that goes against their claims. Today I came across the first case I know of, which appears a short Week-in-Review piece about the woodpeckers in the New York Times. (You have to scroll down a bit to the article.)

First, a conservation biologist is quoted saying that most things that scientists think are extinct are extinct. The article then ends with this:

But Stephen Budiansky, the author of several books on natural history, said the discovery points out how uncertain the business of predicting extinctions of species great and small - mostly small - can be.

All of the big numbers we have heard, of tens of thousands of extinctions worldwide, are not based on field observations," Mr. Budiansky said. "They're based on very simplistic mathematical models. But there's a huge gap between those predictions and the numbers of species we can actually confirm are extinct."

Budiansky's name may be familiar to you, especially if you followed the link to a paper by Stuart Pimm I provided in the last post. In the early 1990s, Budiansky was one of the first people to float the idea that North American birds demolish estimates of the current extinction rate based on habitat loss. Budiansky didn't actually make these claims in a scientific paper, but first in an article for U.S. News and World Report, and then later in a book, Nature's Keepers. In the paper I linked to, Pimm explicitly cites Budiansky's claims, and then proceeds to show that they are wrong. Fast forward some ten years. In that time Budiansky has, as far as I can tell from my search, never responded to Pimm's paper in a scientific journal or magazine. Nevertheless, he's still ready to hold forth about extinctions. I suppose he's trying to be controversial, but from his quote, you'd think that conservation biologists made these mathematical models in some smoke-filled back room and kept them a sworn secret. But you just need to look at Pimm's paper, or any other in this area, to see that they've always been upfront about using mathematical modeling to make predictions--just as a chemist uses mathematical models to make predictions about a chemical reaction, or a meteorologist uses models to predict the weather next week. But there's also been a long tradition of fieldwork (and experiments) to test the assumptions of the model. As for the huge gap between predictions and numbers of species we can actually confirm are extinct, if Budiansky wants to bankroll the millions of field biologists who would be needed to track the fate of all the millions of species on Earth over the next 200 years, I'm sure no conservation biologist would complain. But until then, our knowledge will have to remain imperfect.

(For those who want more: 1. Stuart Pimm gave an interesting talk on all this a couple years ago, and the transcript and audio file are available here. 2. For a similar case of flimsy "skepticism" about extinctions, see this post.)

From time to time, scientists discover that a species that was once thought to have become extinct is actually surviving in some remote place. If the species is a salamander or a lemur, it gets a quick headline and then promptly goes back to its obscure, tenuous existence. But here's one rediscovered creature that I suspect will get some major press: the Ivory-billed woodpecker is back. Science is publishing a paper in which scientists report several sightings and a video of the magnificent bird, which hadn't been seen since in the United States since 1944. Here is a report from the AP.

The challenge of studying extinctions is that it can be hard to know when a species is finally gone for good. If a species of flower lives only on a single bare island the size of a hot-dog stand, you can be pretty sure that if you don't see any of the flowers for a few years, it's gone. But if, as is the case for the Ivory billed woodpecker, a species exists in remote forests and at low density, the failure to see it may just mean scientists haven't looked everywhere. Eventually, most scientists will just give up and presume the animal extinct. As a result, ornithologists and amateur birders have been wondering for decades whether the woodpecker is actually still alive. Incredibly, it is--in some remote woods in Arkansas.

So what does it mean that today the Ivory billed woodpecker seems to be alive? Is it proof that environmentalists have been crying wolf about the dangers of extinction? Do we not need to worry? Is wildlife taking care of itself?

A couple maps can help put the discovery into perspective. This first map shows the original range of the ivory-billed woodpecker. It thrived in mature forests in the southeastern United States, particulary along the coasts and up the Mississippi. The second map shows its range in between 1900 and 1930. The striped regions are habitat that the woodpecker lost between 1900 and 1930. The orange spots were all that was left of its range in 1930.

The reports today do not mean that the woodpeckers are actually living in their former range. They don't even show that the bird exists in its 1930 range. The sightings were all made in the Arkansas patch--a tiny portion of the area in which the woodpecker once lived. The researchers say in their paper that the sightings were made in some 200,000 hectares of Arkansas forest that all might be well-suited to the woodpeckers. Is that cause for optimism? It depends on the biology and ecology of the birds. Will they be able to sustain a healthy population in a relatively small remnant of their original range? That's an open question. It is possible that the woodpecker may also be lurking in other parts of its former range, but that doesn't necessarily boost the species's odds of survival. Such a hypothetical population might well be isolated from the Arkansas population, like two islands separated by hundreds of miles of ocean. If one population disappears due to inbreeding, disease outreaks, or some other disaster, its numbers won't be boosted by immigrants from the other population.

This gets to the heart of the extinction process. Conservation biologists have argued for a long time that as habitats get fragmented, the chances of the species they are home to becoming extinct go up. Given the rate at which forests have been cleared, wetlands drained, and so on, they've warned that we face a massive pulse of extinctions. (Of course, pollution, hunting, invasive species, and other assaults don't help, either.)

Some skeptics such as Bjorn Lomborg have claimed that this is just fear-mongering. They pointed out that of the 200-some species of birds in eastern North America when Europeans arrived with their axes, only 4 were considered extinct--including, at the time, the Ivory-billed woodpecker. Given that the European settlers cleared vast swaths of forests, some simple calculations would suggest that 26 species should have become extinct.

Ten years ago Stuart Pimm, now at Duke, demonstrated that this argument was meritless. In a paper in the Proceedings of the National Academy of Sciences, he pointed out that predictions of extinction based on habitat loss have to take into consideration the range of the species and the extent of the habitat loss. Most of the birds of eastern North America lived across vast expanses. When farmers were cutting down trees in New England, those birds might be living happily in Pennsylvania and Ohio. When the settlers moved to Pennsylvania and Ohio, the birds could still live in Kentucky or Arkansas--and might even start recolonizing the forests that returned to the farmed-out regions of New England. In fact, many species of birds that live in the eastern United States can be found far north in Canada. If you consider only the birds that live in the forests of the eastern United States (between 11 and 28, depending on how strict you make the rules for membership in this club), the rate of extinction has actually been a bit higher than conservation biologists would predict.

I won't be at all surprised if various bloggers and pundits try to turn the rediscovery of the Ivory billed woodpecker into a refutation of the idea that fragmentation leads to extinction. (I'll post links to them if I come across them this week.) But I will be surprised if these pseudoskeptics actually address Pimm's paper. The paper also makes an important point that Pimm has followed up on with more recent research: a lot of the world's biodiversity is very different from the robins and crows and other birds that I see out my window here in Connecticut. A lot of biodiversity is made up of species with relatively small ranges, living in the tropics where forests are currently being wiped out at a rapid rate. These species may be able to hang on for a few decades in relatively large fragments, Pimm argues, but they're waiting out a death sentence. While extinction rates among birds in North America may be relatively low, the same process appears to be causing a catastrophe in the tropics.

It is wonderful that so many people--scientists, government officials, environmental groups, private land owners, and obsessed birders--have helped rediscover the Ivory-billed woodpecker and may be able to help it thrive in one corner of its former range. But this good news shouldn't be misused to distort the big picture.

This morning the New York Times reported that the National Geographic Society has launched the Genographic Project, which will collect DNA in order to reconstruct the past 100,000 years of human history.

I proceeded to shoot a good hour nosing around the site. The single best thing about it is an interactive map that allows you to trace the spread of humans across the world, based on studies on genetic markers. I'm working on a book about human evolution (more details to come), and I've gotten a blinding headache trying to keep studies on Y-chromosome markers in Ethiopian populations and mitochondrial DNA markers on the Andaman islands and all the rest of the studies out there straight in my head. Thank goodness somebody put them all in one place.

Of course, the project is much more than a pretty map: it's an ambitious piece of research. It's basically the brain child of Spencer Wells, a geneticist who wrote the excellent Journey of Man a few years ago. As of now, only about 10,000 people's DNA has been analyzed in studies on human migrations. Wells wants to crank that number up to 100,000. He's going to gather DNA from indigenous populations, and he's also inviting the public to get involved. You can buy a DNA kit, and when you send it back to the Genographic Project, you'll get a report on "your genetic journey" and the information will get added to Wells's database.

When Wells's book came out, I reviewed it for the New York Times Book Review. I gave it thumbs-up for the most part, although I felt that he had glided over the difficult ethical issues involved in these studies. The biotech industry is very interested in them, because they may point the way to new--and potentially profitable--medicines. An isolated population may have a pattern of genetic variation that sheds light on how a disease works its harm, or may have evolved a unique defense against a pathogen. When I wrote my review, Wells was a consultant to Genomics Collaborative, a private Massachusetts outfit that manages a medical collection of DNA and tissue samples from thousands of people around the world. It appears that he no longer is associated with them.

There's nothing wrong with this interest per se, but the fact is that it has led to some serious conficts. Critics have wondered why companies should be able to potentially reap great reward from the DNA of indigenous people, particularly when so many these groups face cultural extinction. DNA collections have in some cases ground to a halt because of these concerns. Wells didn't deal with tricky issues in The Journey of Man, which I thought was a mistake. That sort of omission, I think, only makes people unnecessarily suspicious.

The Genographic Project poses these sorts of ethical challenges once again, and it's good to see that Wells and his colleagues have confronted them head on. They have posted a long FAQ answering some of the big questions. No pharmaceutical companies are paying for the research. Instead, the Waitt Family Foundation has ponied up the cash for the fieldwork (to a total of $40 million), and IBM is supplying technology and PR.. Net proceeds from the sale of kits will go to education and conservation projects directed towards the indigenous peoples Wells will be working with. The identity of the DNA will remain confidential, but the database will not. Instead, it will be made free and public, along the lines of the Human Genome Project, so that any scientist can use it to study disease (or any other relevant question).

I'll bet that in a few years Wells will have another book to write from this experience. I hope that there's room in it this time for the ethics and the politics he's dealing with. That would help show just how relevant the wanderings of our ancestors 50,000 years ago are to our lives today.

Update 4 pm: Bad link fixed.

I have a weakness common to many bloggers--I like to check my site meter to see who's coming to my blog, and from where. Often I wind up discovering intriguing sites run by people whose interests run along the same lines as mine, such as evolutionary biology. Today, however I was surprised to see a lot of traffic coming from Answers in Genesis, a creationist web site.

First off, greetings to all visitors who come through the link. I hope you find some interesting things here.

I decided to investigate the source of the link, and the results were interesting. It turns out that today Answers in Genesis put a new page up in which a writer attacks a recent post of mine about HIV. I explained how recent research on a virulent new strain of the virus relied on evolutionary biology to investigate its origins, and how understanding natural selection helps scientists put together strategies for vaccines, antiviral treatments, and other ways to fight the disease. And I pointed out that creationism appears nowhere in this research, providing no help in understanding this particularly nasty aspect of the natural world.

Answers in Genesis takes pity on me for not having come to them for enlightenment. "Had Zimmer checked this website first, he would have known that far from creationists ducking for cover at this ‘blinding new evidence’ (as his article, especially its title, implies), we wrote an article years ago Has AIDS evolved which, in principle, raised and dealt with the points his piece makes."

It's important to address some of the erroneous claims raised in the piece, but it's not easy because they are mixed together with non sequiturs and other distractions. "Blinding new evidence"--quote unquote? Do those words appear in my blog? No. Does the writer attribute them elsewhere in his piece to someone else? No. He's just putting quotation marks up arbitrarily.

And then there's the claim that the piece he refers to raised and dealt with my points "in principle." The HIV research I'm discussing was published in 2005. The piece in Answers in Genesis came out in 1990. Did the folks at Answers in Genesis know then that this paper on HIV would be coming out in fifteen years? Could they foretell its contents so well that they could explain how creationism would actually guide the research? Again, no.

What Answers in Genesis actually said in 1990 was this: when scientists observe evolutionary change in viruses such as HIV, they have not found proof that viruses evolved into people. "Viruses can have no evolutionary relationship to any other form, and so whatever may have happened to say, the AIDS virus, has no relevance to the supposed history of truly living organisms in any case," Answers in Genesis claims.

To those who find this claim impressive, I would point out a couple things.

First of all, it evades the actual point of my post, which was that scientists who are working on HIV and other pathogens do not base any of their work on creationism of any flavor, including intelligent design. You can look in medical journals all you want, but it's just not there. Mutation, natural selection, genetic drift, and the adaption to new host species are what's there. (See my follow-up post for some research on the deep history of HIV.)

Second of all, it's just flat-out wrong to say that "viruses have no evolutionary relationship to any other form." Scientists have documented many cases in which the DNA in viruses and the DNA in a bacteria, animal, or some other organisms show an evolutionary link. In some cases, viruses have permanently patched themselves into host genomes, including our own. In other cases, viruses appear to have evolved from a segment of DNA from some organism, having acquired mutations that allow them to break free and infect other hosts. In still other cases, the viruses have grabbed host genes along the way, turning into a veritable genetic mosaic. Viruses appear to have been present since the earliest stages of life on Earth and may have given rise to some of our most important celular machinery. A quick search of the scientific literature brings up a wealth of papers addressing the intimate role of viruses in our evolution--here are just a few gems:

Viruses as the source of new genes in bacteria

A catepillar virus that evolved from the wasps that parasitize catepillars.

A look at the entire range of viruses, and a discussion of how viruses may have preceded cellular life.

Another look at how viruses have been inserting themselves in genomes since the origin of cellular life.

An analysis that indicates that some of the most essential enzymes in our cells come from viruses.

A leading evolutionary biologist writes: "I suggest here that DNA and DNA replication mechanisms appeared first in the virus world before being transferred into cellular organisms."

I heartily suggest that people read the Answers in Genesis piece on viruses--not for any scientific enlightenment, but as an example of the bait-and-switch tactics and omission of evidence that's necessary to create the impression that there has to be some "blinding" line dividing small and large scale evolutionary change. (Quotation marks mine!)

On the cover of Nature, the editors splashed the first reconstruction of Sahelanthropus, the oldest known hominid. The scientists who made the reconstruction used new material they found in the Sahara, adding to the material they described in their first report in 2002. There had been some argument over whether Sahelanthropus was an early hominid that looked a lot like other apes, or an ape that had a passing resemblance to hominids. The authors argue the former. They also claim that their new reconstruction provides new evidence that Sahelanthropus may have been bipedal. MSNBC reports that other scientists would prefer to see a nice pelvis or femur before accepting that claim.

Meanwhile, via John Hawks, National Geographic has a lovely display of some of the oldest hominids fossils found outside of Africa. Found in Georgia, they were initially assigned to Homo erectus, which is known to have spread all the way to Indonesia by 1.8 million years ago. But Homo erectus was a tall hominid with a big brain and a relatively flat face. The Georgia hominids, as you can see in NG's new reconstructions, were tiny and reminiscent of earlier hominids back in Africa. Which raises the possibility, which I've discussed before, that the "hobbits" recently found in Indonesia (Homo floresiensis) might have been the relicts of a pre-Homo erectus migration of little folks out of Africa. (NG also has an article on the hobbits this month, by the discoverers.)

Unfortunately, there's also bad new about hominids these days--the hobbit bones, which were "borrowed" last fall, are a mess.

I'm guessing it's only a matter of time before this guy gets a show on cable. Bryan Fry is a biologist at the University of Melbourne in Australia, and he spends a lot of his time doing this sort of thing--messing with animals you really really shouldn't mess with. In addition to being telegenic, he rattles off those delicious Australian phrases, like, "No drama, mate." (Translation: No problem.)

While Fry is comfortable milking a king cobra in a jungle, he also has a lab-jockey side, using genomic technology to dredge up vast numbers of new snake venom genes. In tomorrow's issue of the New York Times, I have an article about Fry's latest research. He has offered a rough draft of the history of venoms--a 60 million year tale of gene recruitment and gene duplications and high-speed evolution. Understanding this history is a crucial part of Fry's long-term goal of turning venoms into new drugs--a tradition that has already given rise to billions of dollars of sales each year and many lives saved. That may put him off-limits for IMAX movies, but television seems inevitable.

Spring is finally slinking into the northeast, and the backyard wildlife here is shaking off the winter torpor. Our oldest daughter, Charlotte, is now old enough to be curious about this biological exuberence. She likes to tell stories about little subterranean families of earthworm mommies and grub daddies, cram grapes in her cheeks in imitation of the chipmunks, and ask again and again about where the birds spend Christmas. This is, of course, hog heaven for a geeky science-writer father like myself, but there is one subject that I hope she doesn't ask me about: how the garden snails have babies. Because then I would have to explain about the love darts.

Garden snails, and many other related species of snails, are hermaphrodites, equipped both with a penis that can deliver sperm to other males and with eggs that can be fertilized by the sperm of others. Two hermaphroditic snails can fertilize each other, or just play the role of male or female. Snail mating is a slow, languorous process, but it also involves some heavy weaponry. Before delivering their sperm, many species (including garden snails) fire nasty-looking darts made of calcium carbonate into the flesh of their mate. In the 1970s, scientists sugested that this was a gift to help the recipient raise its fertilized eggs. But it turns out that snails don't incorporate the calcium in the dart into their bodies. Instead, love darts turn out to deliver hormones that manipulate a snail's reproductive organs.

Evolutionary biologists have hypothesized that this love dart evolved due to a sexual arms race. When a snail receives some sperm, it can gain some evolutionary advantage if it can choose whether to use it or not. By choosing the best sperm, a snail can produce the best offspring. But it might be in the evolutionary interest of sperm-delivering snails to rob their mates of their ability to choose. And love darts appear to do just that. Their hormones prevent a snail from destroying sperm with digestive enzymes, so that firing a love dart leads to more eggs being fertilized.

Recently Joris Koene of Vrije University in the Netherlands Hinrich Schulenberg of Tuebingen University in Germany set out to see how this evolutionary arms race has played out over millions of years. They analyzed DNA from 51 different snail species that produce love darts, which allowed them to work out how the snails are related to one another. They then compared the darts produced by each species, along with other aspects of their reproduction, such as how fast the sperm could swim and the shape of the pocket that receives the sperm.

Koene and Schulenberg found that love darts are indeed part of a grand sexual arms race. Love darts have evolved many times, initially as simple cones but then turning into elaborate harpoons in some lineages. (The picture at the end of this post shows eight love darts, in side view and cross section.) In the same species in which these ornate weapons have evolved, snails have also evolved more powerful tactics for delivering their sperm, including increasingly complex glands where the darts and hormones are produced. These aggressive tactics have evolved, it seems, in response to the evolution of female choice. Species with elaborate love darts also have spermatophore-receving organs that have long, maze-like tunnels through which the sperm have to travel. By forcing sperm to travel further, the snails can cut down the increased survival of the sperm thanks to the dart-delivered hormones.

Sexual conflict has been proposed as a driving force in the evolution of many species, and this new research (which is published free online today at BMC Evolutionary Biology) supports the idea that hermaphrodites are not immune to it. What's particularly cool about the paper is that all these attacks and counter-attacks co-vary. That is, species with more blades on their love darts tend to have longer rerpoductive tracts and more elaborate hormone-producing glands and so on. Only by comparing dozens of species were they able to find this sort of a relationship.

My wife always tells me that as a science writer, I ought to be well-prepared to give our children the talk about the birds and the bees. But I'm not sure the love darts would send quite the right message.

I'll be a guest tonight at 7 PM EST on NPR's talk show On Point, talking about the new wave of dinosaur science. Jack Horner will be on as well, delivering the dirt about his mind-blowing discovery of soft tissue from a T. rex. Should be interesting.

Update, 3/29/05 9:30 am: The show is now archived here. The links to the real player and windows media feeds are at the top of the page.

Today Gregor Mendel is a towering hero of biology, and yet during his own lifetime his ideas about heredity were greeted with deafening silence. In hindsight, it's easy to blame his obscurity on his peers, and to say that they were simply unable to grasp his discoveries. But that's not entirely true. Mendel got his ideas about heredity by experimenting on pea plants. If he crossed a plant with wrinkled peas with one with smooth peas, for example, the next generation produced only smooth peas. But when Mendel bred the hybrids, some of the following generation produced wrinkled peas again. Mendel argued that each parent must pass down factors to its offspring which didn't merge with the factors from the other parent. For some reason, a plant only produced wrinkled peas if it inherited two wrinkle-factors.

Hoping to draw some attention to his research, Mendel wrote to Karl von Nageli, a prominent German botanist. Von Nageli was slow to respond, and when he did, he suggested that Mendel try to get the same results from hawkweed (Hieracium), the plant that von Nageli had studied for decades. Mendel tried and failed. It's impossible to say whether von Nageli would have helped spread the word about Mendel's work if the hawkweed experiments had worked out, but their failure couldn't have helped.

After Mendel's death, a new generation of biologists discovered his work and, with the insights they had gathered from their own work, they realized he had actually been onto something. Pea plants really do pass on factors--genes--to their offspring, and sometimes the genes affect the appearance of the plants and sometimes they don't. Mendelian heredity, as it came to be known, was instrumental in the rise of the new science of genetics, and today practically every high school biology class features charts showing how dominant and recessive alleles are passed down from one generation to the next. Mendelian heredity also helped explain how new mutations could spread through a population--the first step in evolutionary change.

But what about that hawkweed? It turns out that usually Hieracium reproduces very differently than peas. A mature Hieracium does not need to mate with another plant. It does not even need to fertilize itself. Instead, it simply produces clones of itself. If Nageli had happened to have studied a plant that reproduced like peas, Mendel would have had more luck.

Hawkweed raises an important question--one that is particularly important this morning. Does it tells us that Mendel was wrong? Should teachers throw their Mendelian charts into the fire? No. Mendel found a pattern that is widespread in nature, but not a universal law. Most animals are pretty obedient to Mendel's rule, as are many plants. Many algae and other protozoans also have Mendelian heredity, although many don't. Many clone themselves. And among bacteria and archaea, which make up most of the diversity of life, Mendelian heredity is missing altogether. Bacteria and archaea often clone themselves, trade genes, and in some cases the microbes even merge together into a giant mass of DNA that then gives rise to spores.

Today in Nature, scientists found another exception to Mendelian heredity. They studied a plant called Arabidopsis (also known as cress) much as Mendel did, tracing genes from one generation to the next. They crossed two lines of cress, and then allowed the hybrids to self-fertilize for two more generations. Some of the versions of the genes disappeared over the generations from the genomes of the plants, as you'd expect. But then something weird happened: in a new generation of plants, some of the vanished genes reappeared. The authors think that the vanished genes must have been hiding somewhere--perhaps encoded as RNA--and were then tranformed back into DNA.

Is cress the tip of a genetic iceberg (to mix my metaphors hideously)? Only more experiments will tell. If it is more than just a fluke, it may turn out to play an important part in evolution, joining some other weird mechanisms, such as "adaptive mutation," in which bacteria crank up their mutation rate when they undergo stress. But hold onto those Mendelian charts. These cress plants are wonderfully weird--but no more wonderfully weird than hawkweed.

Panda's Thumb has an update on the ongoing drama over teaching creationism in public schools taking place in York, Pennsylvania. Last year a group of residents donated 58 copies of a creationst book called Of Pandas and People to the local school. The board of education reviewed them and gave them the green light. The books are now available in the school library.

Now someone has donated 23 science books, many of which deal with evolutionary biology, to see how the board deals with them. So far, the board has said it will review them as to their "educational appropriateness," and has left it at that.

It's an honor for my book Evolution: The Triumph of an Idea to be on a list that includes work by luminaries such as Stephen Hawking and Ernst Mayr. But if the donor wants to make his point--that evolution is well-established science--even more clearly, I'd suggest adding a few extra items: some of the leading college textbooks in biology, botany, microbiology, genetics, zoology, and developmental biology. Open any of them up and you're likely to find evolution acting as the backbone for all of the knowledge they have to offer. Would the board balk at them? If they did, you'd have to wonder whether they actually want their students to succeed in college.

Readers were busy this weekend, posting over fifty comments to my last post about HIV. Much of the discussion was sparked by the comments of a young-Earth creationist who claims that the evolutionary tree I presented was merely an example of microevolution, which--apparently--creationists have no trouble with. This claim, which has been around for a long time, holds that God created different "kinds" of plants and animals (and viruses, I guess), and since then these kinds have undergone minor changes, but have never become another "kind."

Some readers expressed frustration that the comments were getting side-tracked into arguments about creationism. I take a pretty relaxed attitutde to what goes on in the comment threads, though. Part of that attitude, I'll admit, comes from the fact that I don't have the time to hover over the comments all day. But I also don't relish the thought of shutting down discussion, except of course when comments come from pornography-peddling bots.

I myself find that objections to evolution frequently turn into good opportunities to discuss interesting scientific research. For example, let's take the claim that an evolutionary tree of HIV merely documents microevolution.

Here's the tree from my last post, published in The Lancet. It compares a new aggressive, resistant strain of HIV to strains taken from other patients. These viruses all descend from a common ancestor. The descendants mutated, many mutants died, and some mutants thrived, thanks to their ability to evade the immune systems of their hosts. Strains that share a closer common ancestor fall on closer branches.

This new strain belongs to a group of strains known collectively as HIV-1. What happens if you compare HIV-1 to viruses found in animals? Is it impossible to link these viruses together on a single tree? Were they all created separately, each to plague its own host? That's what one might expect if indeed the "microevolution-yes, macro-evolution no" idea was true. After all, viruses that infect different animals are generally different from one another. They can only survive if they have biological equipment suited to their host species, and different species offer different challenges to a virus.

It turns out that the same approach used to compare HIV strains found in individual people works on this larger scale. Scientists can draw a tree.

Here is the most up-to-date version of the tree, which appears in the latest issue of the Journal of Virology. The different branches of HIV-1 are marked in black. The red branches are viruses known as Simian Immunodeficiency Virus (SIV) found in certain populations of chimpanzees. The blue branches also represent chimp SIV's, but these are more distantly related to HIV-1. (A side note: the Lancet paper doesn't specify exactly which HIV-1 group the nasty new strain belongs to. That's a matter of ongoing research.)

It appears, then, that HIV-1 evolved into a human scourge not once but several times from chimp SIV ancestors. One likely route is the increasing trade in chimpanzee meat in western Africa. Hunters who get chimpanzee blood in their own wounds can become infected, and certain strains that manage to survive in our species can then evolve into better-adapted forms.

Of course, tracing back HIV-1 evolution this far leads to the question, where did the ancestors of HIV-1 come from? The authors of the review in Journal of Virology takes another step back, comparing chimpanzee SIV to SIVs from other monkeys. Does this enterprise now finally collapse? Does "microevolution" finally hit the wall, unable to explain "macroevolution"?

Nope. Here's what they find. The tree on the left is based on studies of one HIV/SIV gene called Pol, and the one on the right is based on another called Env. SIVcpz refers to chimp SIV, and the other abbreviations refer to SIV's found in various monkeys.

It turns out that different genes in chimp SIV have different evolutionary histories. This is no big surprise. Virologists have known for a long time that a single animal can get infected by two different viruses, which--on rare occassion--may combine their genetic material into a single package. The scientists hypothesize that chimp SIV evolved from SIV found in red-capped sooty mangabeys as well as SIV that infects greater spot-nosed, mustached, and mona monkeys. Just as humans hunt chimpanzees, chimpanzees hunt and eat monkeys. So they may have been infected in this manner.

You can take the same walk back in time with any virus that's been studied carefully--or any species of animal or plant. Take us. Scientists publish evolutionary trees all the time in which they compare the DNA of individual people. They also use the same methods to demonstrate that chimpanzees are our closest living relatives, that primates descend from small shrew-like mammal ancestors, that mammals and other land vertebrates descend from fish, and so on. (I don't have time this morning to grab examples of these trees, but if I have time tonight I will.) Certainly there are parts of these trees that are still difficult to make out. DNA sometimes evolves so much that a gene can wind up obscuring its own history, for example. But scientists have never hit the wall that creationists claim exists.

You may have heard last month's news about an aggressive form of HIV that had public health officials in New York scared out of their professional gourds. They isolated the virus from a single man, and reported that it was resistant to anti-HIV drugs and drove its victim into full-blown AIDS in a manner of months, rather than the normal period of a few years. Skeptics wondered whether all the hoopla was necessary or useful. The virus might not turn out to be all that unusual, some said; perhaps the man's immune system had some peculiar twist that gave the course of his disease such a devastating arc. But everyone did agree that the final judgment would have to wait until the scientists started publishing their research.

Today the first data came out in the Lancet. One of the figures jumped out at me, and I've reproduced it here. The scientists drew the evolutionary tree of this new strain. Its branch is marked here as "index case." The researchers compared the sequence of one its genes to sequences from other HIV strains, looking to see how closely related it was to them. The length of the branches shows how different the genetic sequences are from one another. The tree shows that this is not a case of contamination from some other well-known strain. Instead, this new strain sticks way out on its own. The researchers say that they're now working their way through a major database of HIV strains maintained at Los Alamost to find a closer relative.

This tree is a road map for future research on this new strain. It will allow scientists to pinpoint the evolutionary changes caused by natural selection or other factors that made this strain so resistant to anti-HIV drugs. Scientists will also be able to rely on evolutionary studies of other viruses. Often drug-resistant pathogens have to pay a reproductive cost for their ability to withstand attack from our medicines. Under normal conditions, they reproduce more slowly than resistant strains. But scientists have also found that pathogens can then undergo new mutations that compensate for this handicap and make them as nasty as their resistant counterparts. It's possible that the new strain has undergone compensatory mutations, which might make it such a threat.

So here we have evolutionary trees and natural selection at the very core of a vitally important area of medical research. Yet we are told again and again by op-ed columnists and certain members of boards of education that evolution is nothing but an evil religion and that creationism of one flavor or another is the future of science. You'd expect then that Intelligent Design or some other form of creationism would help reveal something new about this HIV. But it has not. That should count for something.

Update: 4/12/05 Greetings, visitors from Answers in Genesis. You may be interested in this new post.

I can't remember the first time I saw the dinosaur fossils at the American Museum of Natural History, but they've been good friends for over thirty years. We've all changed a lot over that time. I've grown up and gotten a bit gray, while they've hiked up their tails, gotten a spring in their step, and even sprouted feathers.

I plan to take my daughters to see the new exhibit at AMNH, Dinosaurs: Ancient Fossils, New Discoveries, this spring, and it will be strange to watch them get to know these dinosaurs all over again. In January I got a chance to slink around the exhibit while it was still under construction when I paid a visit to Mark Norell, the museum's top dinosaur guru. I asked Norell what were the biggest questions he has today about dinosaurs, and we spoke about everything from the evolution of birds to just how wrong Jurassic Park turned out to be. Conversations with him and several other leading dinosaur experts led to my cover story in the new issue of Discover.

Last week my editor at the New York Times asked me to write an article about the evolution of crying, to accompany an article by Sandra Blakeslee on colic. Both articles (mine and Blakeslee's) are coming out tomorrow. As I've written here before, human babies are by no means the only young animals that cry, and there's evidence that natural selection has shaped their signals, whether they have feathers or hair. Among animals, there's a lot of evidence that infants can benefit from manipulating their signals to get more from their parents. On the other hand, evolution may sometimes favor "honest advertisements" that prevent offspring from deceiving their parents. Human crying may be the product of the same conflict of evolutionary interested between parents and children.

This was a tricky article to write, because on the one hand there are some very interesting ideas to examine, but on the other hand, they're only hypotheses that haven't been put to much of a test in humans. I've come across two big papers in the past couple years, this one by Jonathan C.K. Wells in the Quarterly Review of Biology in 2003 and another by Joseph Soltis in the latest issue of Behavioral and Brain Sciences. They offer and evaluate a number of hypotheses for human crying. They even give some thought to colic, that maddening far end of the crying spectrum where perfectly healthy babies cry for hours, turning their parents into shambling wrecks. According to one hypothesis, colic is just a case of deceptive signals from child to mother, carried to an absurd extreme.

These are just preliminary hypotheses, though, and they face a lot of tough tests. As I mention in the article, chimpanzees show no sign of colic, which makes you wonder how deep the evolutionary roots of colic could go if it is not found among our closest living primate relatives. What I didn't have room to mention in the article were some comments published in response to Soltis's paper in Behavioral and Brain Sciences by Hillary Fouts of NIH and here colleagues. They study foraging societies in Africa, and in their years of observing how these people raise kids, they haven't seen any colic either.

One way to account for this pattern is the possibility that colic is a disease of affluence--an adaptation turned maladaptive in the modern age, like a taste for sweets that was once satisfied by fruits and can now be drowned in a sea of high-fructose corn syrup. Wells even suggests that the modern Western food supply may have cut down the cost of crying, making it easier for kids to cry more. In foraging societies, mothers nurse their children up to four times an hour, while mothers in farming and industrial societies nurse their babies far less. Babies also cry to be held (perhaps for warmth and protection from attack), and while foragers hold their babies constantly, Westerners keep their babies separated from them much of the time in cribs, carriages, and car seats. Wells suggests that when a colicky baby sends its cranked-up signal and doesn't get the right response, it cranks up even more.

Again, this is only a hypothesis--a starting point for investigation. Hillary Fouts and her colleagues show what this sort of investigation can look like. In the latest issue of Current Anthropology, they report on a study about the end of crying, comparing how babies respond to weaning in two cultures. Both cultures are found in the same rain forests of the Central African Republic. One group live as foragers, and the others as farmers. The foragers nurse their children many times a day and wean them by gradually taper off nursing. The farmers, on the other hand, cut off their children abruptly--in part because the women need to get back to working in their fields.

Fouts and her colleagues found that the farmer children fussed and cried a lot around the time of weaning, while the forager children didn't show much difference. But the researchers kept following the children and found something interesting: the farmer children stopped fussing before long and then cried a lot less in general. The forager children, on the other hand, kept crying more than the farmer children long after they had been weaned.

Fouts and her colleagues see a subtle strategy at work here. The farmer children may cry in response to weaning because it represents the end of a reliable milk supply and perhaps even because weaning raises the odds of their mothers will get pregnant with another child that will compete for the mother's investment. But once the farmer children are weaned and it is clear that their cries will not do them any more good, they don't waste any further effort on the tears.

The forager children, on the other hand, don't get that clear signal of an impending cut-off, and so they don't fuss and wail more in response. But it's also important to bear in mind that in the foraging community, the children are always around some relative who will be quick to pick up a child. So even after weaning, crying still has some value as a signal, and so the children keep it up.

What I find particularly interesting about this study is that it suggests that we shouldn't use evolution to manufacture a false sense of nostalgia. Just because our ancestors lived in a particular way doesn't mean that the way we live now is automatically bad. Our evolutionary heritage is not completely fossilized; it can in some respects alter itself in response to the conditions in which we grow up. If colic follows this pattern, it is not a cause for collective Western guilt that we don't live as foragers. Instead, it's a call to understand the evolutionary roots of the behavior of our children--both for their well-being and our own sanity.

I've got an article in today's New York Times about animal personalities.

Update: I'm not ashamed to admit I'm a regular visitor to the gossip site Gawker. But I have to say I was surprised to see the personality article turn up there. Will hordes of New York hipsters discover the strange joys of evolution, of comparative psychology? We can only hope.

In my last post, I traced a debate over the evolution of language. On one side, we have Steven Pinker and his colleagues, who argue that human language is, like the eye, a complex adaptation produced over millions of years through natural selection, favoring communication between hominids. On the other side, we have Noam Chomsky, Tecumseh Fitch, and Marc Hauser, who think scientists should explore some alternative ideas about language, including one hypothesis in which practically all the building blocks of human language were already in place long before our ancestors could speak, having evolved for other functions. In the current issue of Cognition, Pinker and Ray Jackendoff of Brandeis responded to Chomsky, Fitch, and Hauser with a long, detailed counterattack. They worked their way through many features of language, from words to syntax to speech, that they argued show signs of adaptation in humans specifically for language. The idea that almost of all of the language faculty was already in place is, they argue, a weak one.

Chomsky, Fitch, and Hauser have something to say in response, and their response has just been accepted by Cognition for a future issue. You can get a copy here. Chomsky, Fitch, and Hauser argue that Pinker and Jackendoff did not understand their initial paper, created a straw man in its place, and then destroyed it with arguments that are irrelevant to what Chomsky, Fitch, and Hauser actually said.

It was exactly this sort of confusion about language that Chomsky, Fitch, and Hauser believe has dogged research on its evolution. The first step to resolving this confusion, they argue, is to categorize the components of language. They suggest that scientists should focus on two categories, which they call the Faculty of Language Broad (FLB), and the Faculty of Language Narrow (FLN). FLN includes those things that are unique and essential to human language. FLB includes those things that are essential to human language but are not unique. They might be found in other animals, for example, or in other functions of the human mind.

Chomsky, Fitch, and Hauser argue that we don't actually know yet what belongs in FLN. The only way to find out is to explore the human mind and the minds of animals. But they argue that the road to an understanding of how language evolved must start here. Simply calling all of language an adaptation is a vague and fruitless statement, and one that leaves biologists and linguists unable to work together.

In their effort to portray language as a monolithic whole utterly unique to humans, Pinker and Jackendoff offer up evidence that Chomsky, Fitch, and Hauser consider beside the point. Consider the fact that the human brain shows a different response to speech than to other sounds. Chomsky, Fitch, and Hauser argue that you can't use the circuitry of the human brain as a simple guide to the evolution of its abilities. After all, some people who suffer brain injuries can lose the ability to read while retaining the ability to write. It would be silly to say that this is evidence that natural selection has altered the human brain because reading provides some reproductive advantage. Animals, Chomsky, Fitch, and Hauser argue, are a lot better at understanding the features of speech sounds than Pinker and Jackendoff give them credit for. In fact, they claim that Pinker and Jackendoff are behind the curve, relying on research that's years out of date. Given all that's been discovered about animal minds, Chomsky, Fitch, and Hauser argue that we should assume that any feature of language can be found in some animal until someone shows that it is indeed unique to humans.

There's a lot that's fascinating in all of the papers I've described in these two posts, but I find them frustrating. Pinker and Jackendoff may have erected a straw man to attack, but I think they can to some extent be forgiven. The 2002 paper by Chomsky, Fitch, and Hauser was murky, and their new paper, which is supposed to clarify it, is a bit of a maze as well. Consider the "almost-there" hypothesis, which they offered up in their 2002 paper. It's conceivable that FLN contains only one ingredient--a process called recursion, which I describe in my first post. If that's true, the evolution of recursion may have brought modern language into existence. On the one hand, Chomsky, Fitch, and Hauser claim to be noncommittal about the almost-there hypothesis, saying that we don't yet know what FLN actually is. On the other hand, they claim there is no data that refutes it. Doesn't sound very noncommittal to me.

I'm also not sure how meaningful the categories of FLB and FLN are. Consider the case of FOXP2, a gene associated with human language. Chomsky, Fitch, and Hauser point out that other animals have the gene, and that in humans its effects are not limited to language (it's important in embryo development, too). So it belongs in FLB, because it's not unique enough to qualify for FLN.

It is true that other animals have FOXP2, but in humans, it has undergone strong natural selection and is significantly different from the versions found in other animals. And just because it acts the human body in other ways doesn't mean that natural selection couldn't have favored its effect on human language. Chomsky, Fitch, and Hauser grant that features of language that belong to FLB may have also evolved significantly in humans. But if that's true, then deciding exactly what's FLN and what's not doesn't seem to have much to offer in the quest to understand the evolution of human language.

For now, the main effect these papers will have will probably be to guide scientists in different kinds of research on language. Some scientists will follow Pinker and Jackendoff, and try to reverse-engineer language. Others will focus instead on animals, and will probably find a lot of new surprises about what they're capable of. But until they come to a better agreement on what adaptations are, and the best way to study them, I don't think the debate will end any time soon.

Earlier this month I wrote two posts about the evolution of the eye, a classic example of complexity in nature. (Parts one and two.) I'd like to write now about another case study in complexity that has fascinated me for some time now, and one that has sparked a fascinating debate that has been playing out for over fifteen years. The subject is language, and how it evolved.

In 1990, Steven Pinker (now at Harvard) and Paul Bloom (now at Yale) published a paper called "Natural Selection and Natural Language." They laid out a powerful argument for language as being an adaptation produced by natural selection. In the 1980s some pretty prominent scientists, such as Stephen Jay Gould, had claimed that the opposite was the case--namely, that language was merely a side effect of other evolutionary forces, such as an increase in brain size. Pinker and Bloom argued that the features of language show that Gould must be wrong.

Instead, they maintained, language shows all the classic hallmarks of an adaptation produced by natural selection. Despite the superficial diversity of languages, they all share a basic underlying structure, which had first been identified by Noam Chomsky of MIT in the 1960s. Babies have no trouble developing this structure, which you'd expect if it was an in-born capacity rather than a cultural artefact.

This faculty of language could not simply be a side-effect of brain evolution, because it is so complex. Pinker and Bloom compared language to the eye. No physical process other than natural selection acting on genetic variation could have produced a set of parts that interacted so closely to make vision possible. And you can recognize this adaptiveness by its similarity--in some ways--to man-made cameras. Likewise, language is made up of syntax, the anatomy for producing complex speech, and many other features. Pinker and Bloom argued that natural selection favored the rise of language as a way for hominids to exchange information--whether that information was about how to dig up a tuber with a stick, or about how a neighboring band was planning a sneak attack. There was nothing unusual about the evolution of language in humans; the same biological concepts could explain it as could explain the evolution of echolocation in bats.

Pinker and Bloom went on to publish a number of papers exploring this idea, as well as some popular books (The Language Instinct and How the Mind Works from Pinker, and Descartes's Baby from Bloom.) But they by no means spoke for the entire community of linguists. And in 2002, one particularly important linguist weighed in: Noam Chomsky.

It was the first time Chomsky tackled the evolution of language in a serious way, which is surprising when you consider how influential he had been on the likes of Pinker and Bloom. He had offered some vague musings in the past, but now he offered a long review in the journal Science, which he coauthored with two other scientists. One was Marc Hauser of Harvard, who has carried out a staggering amount of research on the mental life of primates, and the other was Tecumseh Fitch of St. Andrews University in Scotland, who studies the production of sound by humans and other animals. (You can read more about Fitch's work in an essay I wrote for Natural History.)

The Hauser et al paper is not an easy read, but it has its rewards. The researchers argue that the only way to answer the question of how language emerged is to consider the parts that make it up. They see it as consisting of three systems. Our ability to perceive the sounds of speech and to produce speech ourselves is one (the input-output hardware, as it were). Another is a system for understanding concepts And the final ingredient of language is the computation allows the brain to map sounds to concepts.

Hauser et al see three possible explanations for how this three-part system evolved. One possibility is that all three parts had already evolved before our ancestors diverged from other apes. They introduce this hypothesis and then immediately abandon it like a junked car. The second possibility they introduce could be called the uniquely-human hypothesis: the language faculty, including all its components, has undergone intense natural selection in the human lineage. Pinker and Bloom's argument fits this description. The final hypothesis Hauser et al consider is that almost everything essential to human language can also be found in other animals. Perhaps only a minor addition to the mental toolkit was all that was necessary to produce full-blown language.

The authors point out that a lot of the data that would let them to choose between the three have yet to be gathered. Nevertheless, they devote most of their attention to the almost-everything hypothesis, and it's clearly the one they favor.

They argue that studies on animals already show that they have a lot of the ingredients required for language. Monkeys, for example, can have comprehend some surprisingly abstract concepts. They can understand number and color, for example. As for the input-output hardware for human language, it's not all that special either. Monkeys are so good at recognizing human speech sounds that they can tell the difference between two sentences spoken in different languages. And as for speech production, the researchers argue that the essential anatomy is not unique to humans, either.

Humans, for example, depend on a low larynx to give them the range of sounds necessary for speech. But did the larynx drop down as an adaptation for speech? In an earlier paper, Tecumseh Fitch showed that other species have lowered larynxes, including deer. What purpose does it serve for these nonhumans? Fitch suggests that it began as a way to deceive other animals, by making an individual sound larger than it really is. Human ancestors might have evolved a lower larynx for this function, and only later did this anatomy get co-opted for producing speech.

Hauser et al make a bold suggestion: perhaps only one thing makes human language unique. They call this special ingredient recursion. Roughly speaking, it's a process by which small units--such as words--can be combined into larger units--such as clauses--which can be combined into larger units still--sentences. Because units can be arranged in an infinite number of ways, they can form an infinite number of larger units. But because this construction follows certain rules, the larger units can be easily understood. With recursion, it's possible to organize simple concepts in to much more complex ones, which can then be expressed with the speech-producing machinery of the mouth and throat.

According to the almost-everything hypothesis, all of the components of language may not have all gradually evolved together as an adaptation. Instead, much of it was already in place when recursion evolved. It's even possible, they suggest, that recursion didn't even evolve as part of language, but for another function, such as navigation. By happenstance, it also fit together with the other elements of language and voila, we speak.

The Hauser et al paper got a lot of attention when it first came out, such as this long article in the New York Times. Steven Pinker offered a few cryptic comments about how Chomsky's huge reputation didn't leave much room for those who accepted some of his ideas but dismissed others.

But he would not be content with a couple bite-size quotes. Working with Ray Jackendoff of Brandeis University, he began work on a long reply. It has only now appeared, over two years later, in the March issue of Cognition. (But you can grab it here, on Pinker's web site.) This 36 page retort is remarkable in the sustained force with which it blasts Hauser et al. It's not just a regurgitation of 15-year old ideas; Pinker and Jackendoff marshall a lot of evidence that has only been gathered recently.

While Hauser et al may claim that speech perception is not all that special, Pinker and Jackendoff beg to differ. They point out that we use different brain circuits to perceive speech sounds and nonspeech, and that certain kinds of brain damage can cause "word deafness," which robs people of the ability to perceive speech but not other sounds. Babies also prefer speech to non-speech at an early age, and when they show this preference, language-related parts of their brain become active.

What about speech production? Again, Pinker and Jackendoff argue that humans show signs of adaptation specifically to produce speech. Humans learn to speak by imitation, and are astonishingly good at it. But humans are not good at imitating just any sound. A parrot, on the other hand, can do just as good a job at saying Polly and doing an impression of a slamming door. As for Fitch's ideas about the lowering of the larynx, even if it were true, Pinker and Jackendoff don't think it goes against their hypothesis. Even if the larynx had an earlier function, that doesn't mean that natural selection couldn't have acted on it in the human lineage. Bird wings got their start as feet that reptiles used for walking on the ground, but these limbs obviously underwent intense natural selection for flight.

Pinker and Jackendoff then explore some other aspects of language that Hauser et al didn't address at all. The first is the fact that language is built from a limited set of sounds, or phonemes. Phonemes are crucial to the infinite capacity of language, because they can be combined in so many ways. But they also require us to understand rules about how to pronounce them. Pinker and Jackendoff illustrate this with the phoneme -ed: in the words walked, jogged, and patted it has the same meaning but has three different pronunciations. As far as Pinker and Jackendoff can tell, primates have no capacity that can be compared to our ability to use phonemes. As for why phonemes might have evolved in the ancestors of humans, they point to some fascinating models produced by Martin Nowak of Harvard. Nowak argues that natural selection would favor just a few phonemes because they would be easy to distinguish from one another. Human language lets us say thousands of words without having to understand thousands of individual speech sounds.

Research on language genes are also consistent with a uniquely-human hypothesis, according to Pinker and Jackendoff. A gene called FOXP2, for example, is essential for language, and any mutation to it causes difficulties across the board, from articulating words to comprehending grammar. What's more, comparisons of the human FOXP2 gene with its counterparts in other animals shows that it has been the target of strong natural selection perhaps as recently as 100,000 years ago. If the only new feature of language to evolve in humans was recursion, then you would not expect FOXP2 mutations to do anything except interfere with recursion. They also point out that broad comparisons of the genes in humans, chimps, and mice, suggest that some genes involved in hearing may have undergone intense natural selection in our lineage. It's possible that these genes are involved in speech perception.

Pinker and Jackendoff even take issue with the one part of language that Hauser et al granted as being unique to humans: recursion. Recursion is just a basic logical operation, which you can find not just in human language but in computer programs and mathematical notation. But all humans have a capacity for one special sort of recursion: the syntax of human language. Pinker and Jackendoff declare that the case for the almost-everything hypothesis is "extremely weak."

At this point, I might have expected their rebuttal to come to a close. But instead, it takes a sudden turn. Pinker and Jackendoff find it puzzling that Chomsky would offer the almost-everything hypothesis when the facts go against it and when Chomsky himself had laid the groundwork for the uniquely-human hypothesis. For an answer, they burrow into Chomsky's head. They offer a survey of Chomsky's last decade of research, which has been dedicated to finding the indispensable core of language. As Pinker and Jackendoff describe it, Chomsky's search has led him to a single operation that combines items, which I'll nickname "Merge."

I won't go into all the details of their critique here, but the upshot is that Pinker and Jackendoff aren't buying it. By reducing the essence language to repeated rounds of Merge, Chomsky has to push aside all the things about language that linguists have been spending decades trying to figure out, such as phonemes and the order of words in sentences. The reason that they bring up Chomsky's recent work (which Chomsky calls the Minimalist Program) is because they think it is the source of his views on the evolution of language. Our pre-language ancestors may have simply been missing one thing: the Merge operation.

Pinker and Jackendoff are appalled by this. In fact, they hint that some of Chomsky's ideas about language have a creationist ring to them. Chomsky has said in the past that in order for language to be useful at all, it has to be practically perfect. How then, he wonders, could it have evolved from simpler precursors? Chomsky even likens language to a bird's wing, writing that "a rudimentary wing, for example, is not "useful" for motion but is more of an impediment. Why then should the organ develop in the early stages of evolution?"

"What good is half a wing?" is a question often asked by those who reject evolution. But it is a question with several possible answers, which scientists are currently investigating. Feathers may have evolved initially as insulation. Even stumpy wings could have helped feathered dinosaurs race up into trees, as it helps birds today. Likewise, Pinker and Jackendoff argue that language evolved gradually to its most elaborate form. In fact, imperfect languages still exist. Pidgins allow people to communicate but lack fixed word order, case, or subordinate clauses. Pinker and Jackendoff argue that modern language may have emerged from an ancient pidgin through evolutionary fine-tuning.

In sum, Pinker and Jackendoff conclude, their ideas about the origin of language fit with the evidence from both linguistics and biology, and those offered by Chomsky, Fitch, and Hauser don't.

Now what? Do we have to wait another two years to see whether Chomsky, Fitch, and Hauser crumble under this attack or have something to say in response?

As I'll explain in my next post, the answer, fortunately, is no.

In my last post, I went back in time, from the well-adapted eyes we are born with, to the ancient photoreceptors used by microbes billions of years ago. Now I'm going to reverse direction, moving forward through time, from animals that had fully functioning eyes to their descendants, which today can't see a thing.

This may seem like a ridiculous mismatch to my previous post. We start out with the rise of eyes, a complex story with all sorts of twists and turns, with gene stealing, gene borrowing, gene copying; and then we turn to a simple tale of loss, of degeneration, of a few genes mutating the wrong way and--poof!--billions of years of evolution undone.

In fact, loss is never such a simple matter. I can illustrate this fact with two disparate beasts: fleas and cavefish.

Cavefish were familiar to Darwin, as were the many other blind cave dwellers, such as salamanders and insects. Darwin saw cavefish as yet another example of an animal carrying around the vestiges of its ancestors, just as we carry around the stump of a tail. As for how cavefish lost their eyes, he set natural selection aside. Darwin could not imagine how a fish in a cave would get any benefit from eyes that did a worse job than its ancestors' eyes. "I attribute their loss soley to disuse," he wrote. By disuse, Darwin may well have been thinking along the lines of his precursor, Lamarck. As fish stopped relying on their eyes in the dark, somehow their eyes degenerated, and that degeneration was passed down to the next generation of fish.

Once scientists began to decipher the molecules of heredity, such an explanation became obsolete. Instead, some scientists translated the notion of "disuse" into the language of mutations. Like any animals, a cavefish has a small but real chance of undergoing a mutation to its DNA. In some cases, these mutations can impair the fish's eyes. In a population of surface-dwelling fish, this sort of mutation would probably make it hard for a fish to find food, and might even make it an easy target for predators. The chances of the fish passing down that mutant gene to a new generation of fish would be pretty slim. But in a cave, such a mutation would have no effect on the reproductive fortunes of a fish. Over time, the population of cavefish would accumulate lots of eye mutations, until their eyes were rendered useless.

But this "neutral mutation" hypothesis isn't the only possibility. Scientists have also proposed an "energy conservation" hypothesis. Mutations that prevent cave fish from developing eyes let them save energy, boosting their odds of survival.

Scientists have tested this hypothesis in recent years by studying the fish Astyanax mexicanus. You can find perfectly normal populations of this fish in surface waters in the U.S. , but if you go into caves, you can also find some 30 populations that are blind. This transformation has happened overnight, biologically speaking: scientists estimate that it was only 10,000 years ago that populations Astyanax moved into the caves. One vivid demonstration of just how recent this move was is the fact that a cave fish and a surface fish can mate and produce healthy hybrids. The lion's share of research on Astyanax has been carried out in the laboratory of William Jeffery at the University of Maryland, and he offers an excellent summary in a paper in press in the Journal of Heredity.

Much of Jeffery's work has gone into tracking the development of the fish from eggs. The most startling thing he has found is that cavefish grow eyes for quite a long time. Just as in surface fish, the brains of cave fish embryos bulge out to the sides, stretching into stalks that end in cups. A simple retina and lens begin to form, and growing nerves begin to link the retina to the visual centers of the fish brain. After about a day, however, the cavefish eye and surface fish eye begin to take different paths. The cave fish eye fails to develop an iris or a cornea, for example. Still, many parts of the cave fish eye continue to grow as their cells multiply.

These findings alone call into question both the neutral mutation hypothesis and the energy conservation hypothesis. If mutations were building up in the cave fish genome, you wouldn't expect that the fish could advance so far in the development of their eyes. And if energy conservation was the sole advantage driving the evolution of blindness, you wouldn't expect the fish to keep producing new eye cells, even as the eye begins to deteriorate.

Even the degeneration of the eye challenges both of these hypotheses. The eye doesn't collapse into a stew of chaos; it is dismantled in a stately choreography. The cells in the lens release some signal that instructs other eye cells to begin to commit suicide. In surface fish, the lens sends signals that do just the opposite, allowing the eye to develop fully. Jeffery and his colleagues found that if they transplanted just the lens of a surface fish into the eye of a cave fish, the cave fish grew a completely normal eye. What's more, the transplant triggered new nerve fibers to project from the retina to the brain, and the part of the cave fish's brain that handles vision even grew. It's possible that a transplanted lens allows a cave fish to see. Despite being blind, the cavefish still retains its original circuit of eye-building genes.

Jeffery and his colleagues have also tracked the degeneration of the eye at the level of genes. The neutral mutation hypothesis would lead you to expect that cave fish would express fewer genes in the eye than surface fish, because many of them would have been destroyed by mutations. But this is not the case, Jeffery and his colleagues have found. Instead, they're starting to identify some genes that make more of their proteins in the eyes of cave fish than in those of surface fish, and even some genes that aren't active in the eyes of surface fish at all.

One particularly important protein in the developpment of cavefish eyes is known as Hedgehog. In all vertebrates, Hedgehog plays a vital role in the development of the eye, starting at its earliest stage. Initially, the cells that will give rise to the eyes form a single cluster. Cells in the midline of the embryo start producing Hedgehog, which somehow signal the cells in the middle of this eye cluster to stop developing. As a result, only the cells on the far sides continue to develop, thus producing two separate eyes. Mutations that interfere with the production of Hedgehog can cause a gruesome birth defect in humans called cyclopia, in which a single cyclops-like eye develops.

Cave fish have evolved in the opposite direction: they produce more Hedgehog, rather than less. The extra protein stops the development of a wider expanse of the original eye-cell cluster, leaving few cells to progress. Jeffery and his colleagues confirmed this by boosting the production of Hedgehog in surface Astyanax. Not only do they develop smaller eyes, but they suffer the same lens-directed degeneration seen in cavefish. This means that the degeneration of cavefish eyes requires cells beyond the eyes to help coordinate the process.

What's most remarkable about this choreography is that it has evolved again and again. Studies on Astyanax DNA suggest that populations of surface fish have repeatedly invaded caves, and each time they have gone blind. Jeffery and his colleagues have started comparing the development of embryos from different populations, and they find the cavefish have evolved blindness through the same patterns of gene activity.

This parallel evolution is hardly what you'd expect from a random blast of neutral mutations. Nor does Jeffery believe that energy conservation can explain it. Males and females show no difference in the development of their eyes, despite the fact that females need a lot more energy to make their eggs. Likewise, some populations of cave fish get lots of energy because they live under colonies of bats that can drop food and guano into the water. Despite this luxurious conditions, these fish are no different than their leaner cousins.

Jeffery thinks that Hedgehog may be the key to understanding what's really driving the evolution of cavefish. Like many genes involved in development, Hedgehog has many different jobs. It is known to be essential for the development of tastebuds, for example, as well as teeth and the bones that make up the head. And in cave fish, all of these features are significantly different from surface fish. It's possible that these changes are adaptations that help the cave fish feed more efficiently. These changes were only made possible by cranking up the production of Hedgehog. A side effect of this increase was the destruction of the cave fish eyes. But because eyes aren't essential in the dark, this wasn't such a big price to pay. If Jeffery is right, Darwin's real mistake with cave fish wasn't falling back on a Lamarckian explanation. It was not recognizing how powerful natural selection could be.

Jeffery and his colleagues have managed learned so much about the evolution of cavefish eyes because they figured out how to turn Astyanax into a laboratory organism, which can be studied as carefully as a fruit fly or a lab rat. This sort of transformation takes many years, and only a few species have what it takes. Many other animals have lost their eyes, but in most cases, scientists can only glean less direct clues. Still, the stories they have to tell can be just as interesting. Most interesting of all is the fact that different evolutionary forces seem to have been at work.

Case in point: fleas.

Scientists know very little about the vision of fleas. As insects, fleas have inherited the standard insect eye, which consists of slender columns tightly packed together. But this standard insect eye has undergone drastic changes in fleas. Some fleas have what look like simple eyespots. Others seem to lack any eye at all. To learn about this transformation, a team of biologists from Brigham Young University have compared fleas to their relatives, which still have eyes.

This wouldn't have been possible even a few years ago, because scientists have only recently worked out the "flea tree." Fleas evolved from a group of insects with particularLY sharp vision. Their cousins include scorpionflies, which rely on their image-forming eyes to help them scavenge dead insects. Their closest relatives are "snow fleas" (Boreidae). These wingless insects live in mountains, where they feed on moss. They have small eyes, but can see well enough to jump away if you try to catch them. So it appears that fleas are the product of a long-term evolution towards simpler eyes.

The scientists used this tree to track the evolution of some of the molecules that are essential for vision. Known as opsins, they respond to light by triggering a chemical reaction that sends a signal from the eye to the brain. Opsins can be sensitive to different colors, depending on their shape, which depends in turn on the DNA sequence in their genes. The scientists isolated the gene for green opsins from 11 species of scorpionflies, snow fleas, and true fleas.

The scientists then compared the DNA sequences for signs of change. A mutation to an opsin gene may have no effect on the opsin molecule itself, or it may alter its structure dramatically. The difference depends on where in the DNA sequence that mutation strikes. The scientists found that most changes that occurred during the evolution of fleas had no effect on the actual opsins. They confirmed this by using the DNA sequence of the opsin genes to create computer models of the opsin molecules themselves. Even in fleas, the green opsin molecule has basically the same structure as in scorpionflies--despite their radically different eyes.

Just because a gene hasn't changed for millions of years doesn't mean that it hasn't been experiencing natural selection. The scientists found evidence that the opsin gene has been experience a special kind of natural selection in fleas and their relatives, known as purifying selection. Purifying selection occurs if even the slightest change to the structure of a molecule puts a serious dent in the reproductive success of an animal. The fact that fleas have experience purifying selection on their opsin gene means that it remains essential to their survival. (The details of their work appear in a paper in press at the journal Molecular Biology and Evolution.)

So what on Earth are the fleas doing with their opsins? The scientists doubt that the fleas are using them in their eyes. They point out that flea eyes are covered over in a tough layer of chitin, and they lack the lenses and other structures that would let them see. But in many animals, ranging from pigeons to salmon to butterflies, opsins have also been found outside the eye. In some animals, they grow inside the brain, while in others they grow on the abdomen or other parts of the body. Recent studies suggest that these opsins set the pace for biological clocks by registering the change of light from day to night.

This brings us back around to the very origin of eyes, which I described in my first post. Long before full-fledged eyes evolved, light-sensitive molecules may have existed in microbes, allowing them to change their movements during night and day. These molecules may have been incorporated into early eyes, making it possible for animals to see. But this transition didn't mean that photoreceptors could no longer serve their original function. Early insects may have used opsins both within their eyes to see and outside of their eyes as biological clocks. Later, some lineages of insects lost their eyes. Some may have lost them in dark caves. Fleas, on the other hand, lost their eyes as they became parasites. Instead of navigating through a complex landscape in search of a particular prey, they just hopped from one host to the next. But they still relied on opsins to run their biological clocks. The authors point out that scientists have also found opsins in other animals that have lost their eyes. The animals? None other than Astyanax.

What's particularly remarkable about the new study is how strongly the flea opsin resisted any evolutionary change--even after it was no longer being used in the flea eye. The molecule need the same functional structure for both jobs. As I mentioned at the beginning of my previous post, Charles Darwin recognized that the complexity of the eye might appear to pose a major challenge to his theory. To some people, it still does; they argue that the components of the eye cannot function on their own, and so they could never have existed on their own. By this reasoning, it would be impossible for one of these components--an opsin, for example--to do anything useful if it wasn't inside an eye.

The flea apparently sees things differently.

(The first of a two-part post)

The eye has always had a special place in the study of evolution, and Darwin had a lot to do with that. He believed that natural selection could produce the complexity of nature, and to a nineteenth century naturalist, nothing seemed as complex as an eye, with its lens, cornea, retina, and other parts working together so exquisitely.The notion that natural selection could produce such an organ "seems, I freely confess, absurd in the highest possible degree," Darwin wrote in the Origin of Species.

For Darwin, the key word in that line was seems. He realized that if you look at the different sort of eyes out in the natural world, and consider the ways in which they could have evolved, the absurdity disappears. The objection that the human eye couldn't possibly have evolved, he wrote, “can hardly be considered real.”

The more scientists study the eye, the more they recognize that Darwin was right. This is not to say that they know everything about how the eye evolved. Evolutionary biology is not an automatic answer machine that can instantly tell you every detail about how eyes--or any other organ--evolved. Instead, scientists study eyes of different animals, the proteins they are made of, and the genes that store their recipe. They come up with hypotheses about how evolution could have produced these results. Those hypotheses then point the way to new experiments. In this way, evolutionary biology is no different from geology or meteorology, or any other science that illuminates the natural world.

To be precise, I should say that scientists study the evolution of "the eye." There are millions of different eyes (and other light-detecting organs), each built by a different species from its own unique set of genes. Closely related animals tend to have similar eyes, because they descend from recent ancestors. Some scientists study how eyes can adapt over a few million years to the special circumstances of a particular species. Other scientists step a little further back, to look at how the different types of eyes have evolved from simpler precursors. And other scientists step even further back in time, to find clues about where those simpler precursors came from. In this post, I will move back through time through these different stages of eye evolution (a la Richard Dawkins's The Ancestor's Tale.)

Humans have what's known as a camera eye. Light first passes through a cornea, which refracts the light. It then passes through a lens, which refracts the light further, so that it forms a focused image on the retina. We are primates, and so it's not surprising that all other primates have a similar type of eye. But different primates have important differences in the shape of their eye. Nocturnal primates have wider, more curved corneas than primates that are active during the day. A wider cornea lets nocturnal primates make the most of the moonlight by allowing more of it into the eye. Primates active during the day benefit from small flat corneas probably because the lens can sit further forward in the eye, producing a sharper image. This arrangement doesn't let as much light in, but during the daytime, that's no great loss. Chris Kirk of the University of Texas analyzed primate eyes in the December 2004 issue of The Anatomical Record (he has posted the paper on his web site).

For the most part, nocturnal and diurnal primates fit the same patterns as other mammals. But monkeys and apes (including humans) turn out to have extremely small, flat corneas, even compared to other primates that are active in the daytime. Kirk argues that this particular group of primates (called anthropoids) has experienced natural selection that has produced even sharper vision than found in other mammals active in the daytime. Other aspecsts of the anthropoid eye also make it sharp, including its fovea, a small spot on the retina that's incredibly dense with photoreceptors. In fact, anthropoids are matched only by raptors for their sharp vision. It's possible that our ancestors evolved such sharp eyes for hunting insects; monkeys and apes are also extremely social animals, and they rely on their keen eyes to look at one another and pick up subtle cues in their faces. Our ability to make sophisticated tools may have been made possible by the evolution of tiny corneas.

Changing the shape of an eye requires changing the molecules that make it up. Molecular fine-tuning can also alter an eye's ability to block out UV rays, to refract light at different angles, or to become more sensitive to different colors. Despite the fact that all vertebrates share the same basic eye plan, you can find a wide range of molecules inside them. Some are found only in fish, some only in lizards, some only in mammals.

How does one group of animals evolve one of these new molecules? One way is to borrow it. Joram Piatigorsky of the National Eye Institute and his colleagues have identified many of the molecules that make up the lens and cornea of humans and other animals. These molecules are practically identical to molecules found elsewhere in the body. Some are essential for the development of the head in an embryo. Others protect our cells from heat and other stress, others detoxify poisons that would otherwise build up in the blood.

Originally, the evidence indicates, many of the molecules found in eyes today were only produced in other parts of the body. But then, thanks to a mutation, the same gene began producing its molecule in the developing eye. It just so happened to have the physical properties that made it well suited to being in an eye. In later generations, natural selection favored mutations that made it work better in the eye.

But this new job in the eye may have posed a trade-off for the molecule's original job. Further fine-tuning may have only been possible when the gene went through a particularly drastic (but common) mutation: it duplicated. Now one copy of the gene could adapt to the eye, while the other continued specializing in its original job. (I wrote an essay a couple years ago about some of Piatigorsky's work in Natural History.)

Darwin didn't know about gene sharing or gene duplication, but he still managed to make some important observations about how the human eye could have evolved from a simpler precursor. Early eyes might have been nothing more than a patch of photosensitive cells that could tell an animal if it was in light or shadow. If that patch then evolved into a pit, it might also have been able to detect the direction of the light. Gradually, the eye could have taken on new functions, until at last it could produce full-blown images. Even today, you can find these sorts of proto-eyes in flatworms and other animals.

The closest invertebrate relatives of vertebrates fit nicely into Darwin's predictions. Amphioxus, which looks like a sardine with its head cut off, lacks a true brain or camera eyes. But the front end of its nerve cord is slightly swollen, and is built by many of the same genes that build a human brain. What's more, they grow a pit lined with light-sensitive cells which they seem to use to navigate through the water. The genes that build this pit are nearly identical to the ones that build our own.

The fact that Aphioxus has such a simple precursor to the vertebrate eye might suggest that this organ evolved from scratch. Yet eyes can be found on many other animals--which was how Darwin first figured out what a precursor to the vertebrate eye might have looked like. Eyes can found in insects, squid, and many other animals. Did they evolve independently?

The answer is yes and no. In the 1990s, Walter Gehring of the University of Basel and his colleagues discovered an essential eye-building gene called Pax-6 that was shared by insects and humans. If he inserted the human version of the gene into a fly larva, he got fly eyes popping up all over the fly's body. Gehring has proposed that Pax-6 is a master control gene, switching on an entire circuit of eye-building genes. In insects and in humans (and in all of the animals that share a common ancestor), this circuit builds eyes. But in each lineage, a different set of genes have been incorporated into this circuit, so that they can build eyes as different as the compound eye of an insect and the camera eye of a human.

The simplest explanation for so many animals sharing this same circuit is that they all inherited it from their common ancestor--a small worm-like creature known as a bilaterian that might have lived 570 million years ago. Exactly what sort of eye these genes produced in the Precambrian mists of time isn't clear, though. And until last fall, another feature of the eye didn't seem to fit this hypothesis: its photoreceptors. Invertebrate eyes and vertebrate eyes use different photoreceptors to sense light. But researchers have found that both kinds of photoreceptors grow on a humble animal known as a ragworm, which is believed to have branched off very early in the evolution of bilaterians. It's possible that the ancestor of living bilaterians produced both kinds of photoreceptors. One kind was lost in the vertebrate lineage, and the other was lost in the lineage that led to insects and other invertebrates with full-blown eyes.

Yet eyes are not limited to bilaterians. Jellyfish belong to a branch of animals known as cnidarians that split off from the ancestors of bilaterians some 600 million years ago. Some species have simple photoreceptors, while others have full-blown camera-eyes hanging from their tentacles. Biologists want to know whether these eyes evolved independently, or share some of the ancestral toolkit that produced human eyes and fly eyes. One hint that they share a common heritage is the fact that some of the genes that jellyfish use to build eyes bear a striking similarity to Pax-6 and other genes that build bilaterian eyes. On the other hand, most cnidarians (such as sea aneomones and corals) don't have eyes. What's more, jellyfish eyes are pretty weird compared to bilaterian eyes--for one thing, they don't wire up to a brain. The larvae of one species grow photoreceptors that don't even connect to a neuron. The photoreceptors link instead to hair-like structures in the same cell. Presumably light triggers these cells to flail their hairs to make the larva swim.

In years to come, the search for the roots of eye evolution will push even further back in time. In a paper in press at the Journal of Heredity, Walter Gehring points out that the first component of animal eyes to have evolved was the photoreceptor--a molecule that could catch light and turn it into a signal. One model for the origin of animal photoreceptors comes from colonies of algae, many of which have "eyespots" that allow them to swim towards the light so that they can photosynthesize. Perhaps early animals lived in colonies as well and had similar eyespots. Later, these simple photoreceptors evolved pigments and other molecules that helped capture more light, and eventually became able to form images.

But Gehring also proposes a weird but compelling alternative: our ancestors stole their eyes. Many times over the course of evolution, organisms have been engulfed by larger organisms, and the two have become integrated into a single being. Our cells, for example, contain mitochondria that we rely on to generate energy; originally, these were free-living oxygen-consuming bacteria. Another important fusion took place over two billion years ago, when bacteria that could carry out photosynthesis were consumed by an amoebae-like host. The bacteria then became a structure called the chloroplast, which can be found today in trees and other plants, as well as various sorts of algae. Increidbly, some of these algae were engulfed by other algae, which also came to depend on the photosynthesis carried out by the bacteria. Gehring likens these organisms to Russian dolls, with the original bacteria nestled deep within other organisms.

It's likely that before the bacteria were consumed again and again, they had already evolved a light-sensing molecule that helped them harness sunlight--perhaps by acting as a biological clock. The algae that devoured the bacteria may have retained the ability to sense light for the same purpose. Gehring points out that one group of these algae--dinoflagellates--have fused with corals, jellyfish, and other animals. It's possible that early animals may have incorporated the genes for light-sensing in their own genomes. If he's right, we gaze at the world with bacterial eyes.

Coming next: Once the eye evolves, what does it take for it to disappear?

Over the next week or so, I'm going to post a couple two-part posts. I've gotten mildly obsessed with two big topics in evolution: eyes and language. There's been so much fascinating work done on both subjects in the past year or so that a single post just won't do for either of them. I know that the blog genre lends itself well to quick hits, but I'm going to stretch things a bit. We'll see how it works.

Readers of the Loom may recall an earlier post about how creationists (including proponents of Intelligent Design) misleadingly cite peer-reviewed scientific research in order to make their own claims sound more persuasive. I mentioned that when the scientists themselves find out their research has been misrepresented, they groan and protest.

In case you thought I was exaggerating, check out National Academy of Science president's Bruce Albert's letter to the editor of the New York Times in response to Michael Behe's recent creationist Op-Ed. Behe quoted Alberts describing his early impressions of the cell as a beautiful machine--which Behe takes as evidence that it really is a machine built by someone.

Alberts responds:

In “Design for Living” (Op-Ed, Feb. 7), Michael J. Behe quoted me, recalling how I discovered that “the chemistry that makes life possible is much more elaborate and sophisticated than anything we students had ever considered” some 40 years ago. Dr. Behe then paraphrases my 1998 remarks that “the entire cell can be viewed as a factory with an elaborate network of interlocking assembly lines, each of which is composed of a set of large protein machines.”

That I was unaware of the complexity of living things as a student should not be surprising. In fact, the majestic chemistry of life should be astounding to everyone. But these facts should not be misrepresented as support for the idea that life's molecular complexity is a result of “intelligent design.” To the contrary, modern scientific views of the molecular organization of life are entirely consistent with spontaneous variation and natural selection driving a powerful evolutionary process.

In evolution, as in all areas of science, our knowledge is incomplete. But the entire success of the scientific enterprise has depended on an insistence that these gaps be filled by natural explanations, logically derived from confirmable evidence. Because “intelligent design” theories are based on supernatural explanations, they can have nothing to do with science.

Bruce Alberts
President
National Academy of Sciences

Nuff said.

[Thanks to Pharyngula among others.]

Growing up as I did in the northeast, I always assumed that the really weird life forms lived somewhere else--the Amazonian rain forest, maybe, or the deep sea. But we've got at least one truly bizarre creature we can boast about: the star-nosed mole. Its star is actually 22 fleshy tendrils that extend from its snout. For a long time, it wasn't entirely clear what the moles used the star for. The moles were so quick at finding food--larvae, worms, and other creatures that turn up in their tunnels--that some scientists suggested that the star could detect the electric fields of animals.

That idea hasn't panned out, but the truth has turned out to be just as exotic. As I write in tomorrow's issue of the New York Times, the star is the most sensitive touch organ known to science. It is studded with 25,000 touch-sensitive nerve organs, which channel their sensations into 100,000 large nerve fibers (more than in your entire hand). These nerves then carry the signals to the brain, much of which is dedicated to interpreting what the star feels. As Ken Catania of Vanderbilt University reports in a paper appearing in the current issue of Nature, this heavy-duty wiring produces record-setting speed. As soon as the star-nosed mole comes into contact with food, it needs a fifth of a second to gobble it down. (The article includes a sequence, of frames from one of these filmed feasts.)

As some readers of the Times may notice, this mole article appears in the science section a day after an op-ed column appeared in the editorial section promoting Intelligent Design. Michael Behe, a Lehigh University biologist, claims that evolutionary biologists have not offered hypotheses for how complex things evolve in nature. Given this supposed lack of explanations, and given the supposedly obvious signs of design in biology, Behe concludes that life must be the product of an Intelligent Designer.

Behe is incorrect. In fact, evolutionary biologists have put together hypotheses for many complex systems, which they have published in leading peer-reviewed biology journals. The immune system is one example, which I blogged about in December. The star of the star-nosed moles is another. Ken Catania's hypothesis for its origin starts with the observation that the star is not quite as unique as it may seem at first sight. The touch-sensitive organs it uses (called Eimer organs) are found on the noses of other moles, albeit it in far lower densities. What's more, coast moles, close relatives of star-nosed moles, have small, pipe-shaped swellings at the very tip of its nose, which resemble the star on a star-nosed mole when it is still an embryo.

The star, Catania argues, evolved on a coast-mole-like ancestor. The swellings became larger, the nerves became denser, and the brain dedicated more space to processing the star's signals. Natural selection favored this trend, according to Catania, because the star-nosed moles moved from dry habitats to wetlands, which are loaded with small insect larvae. In addition to big insects, such as earthworms or crickets, star-nosed moles added these small prey to their diet. The star provided benefits to the mole long before it had taken the full-blown form it has today. The more time the star-nosed moles shaved off their performance, the more calories they could take in each second.

Catania's hypothesis takes into account all of the evidence he and others have gathered about star-nosed moles--their behavior, the microscopic structure of their star, the architecture of their brains, their ecology, and the same evidence in closely related moles. It builds on what scientists already know about variation, inheritance, and natural selection. As a hypothesis, it's open to testing, based on further observations of star-nosed moles and their relatives. And that's what Catania is doing.

As for corresponding published papers that use Intelligent Design to interpret the star-nosed mole, they do not exist. The closest I can find are some comments from Answers in Genesis. On their web site, they claim that Catania's hypothesis cannot be right because it is based on "the discredited idea of Embryonic Recapitulation." This claim is based on the fact that the nineteenth century biologist Ernst Haeckel doctored some pictures of embryos in order to fit his own notion about how evolution progressed in certain directions. Nevertheless, the scientific consensus today--based on over a century of research since Haeckel's day--holds that changes in the way embryos develop can lead to dramatic evolutionary change (Here's a good account of the current undertanding.).

The Answers in Genesis site then asks, "Why would a ‘primitive’ mammal suddenly start to develop such a specialized appendage? If it was already successfully hunting food without the star, what was the evolutionary ‘trigger’ for the star’s development?" Catania has already laid out this part of his hypothesis: the ancestors of star-nosed moles moved into wetlands, where variations that helped them feed on insect larvae could get them more food and boost their odds of reproducing. Other mole species, living in dry soil, didn't have this incentive. What's more, the delicate star would be damaged scraping against the hard tunnels dug by other moles.

These are some of the reasons why Catania and other scientists that I interview are not swayed by the sorts of claims made by Answers in Genesis or Michael Behe (as evidenced by the lack of peer-reviewed papers that they have inspired). Instead, what excites these scientists are the common themes that arise when they study the origins of different complex traits. Consider, for example, the adaptive immune system. I won't go into detail here about the latest thinking about how it evolved (I already have here). But I will point out that it seems to have followed the same trajectory as the star-nosed mole. It did not come out of nowhere. Parts of the system--including organs, cells, and receptors, were already in place millions of years earlier, often serving different functions than they do today. These parts were then modified, connected together in new ways, and gradually took on the form they have today. The same goes for the star-nosed mole and many other case studies in complexity--even including artificial life.

In the interest of full disclosure, I cannot end this post before confessing that the evolution of complexity was not the only thing I found fascinating in working on this article. Searching for a point of comparison for the speed of star-nosed moles, I wound up at the web site for the International Federation of Competitive Eating. Did you know someone holds the record for eating cheesecake? Eleven pounds in nine minutes. Now that's bizarre.

Thanks to the many people who left comments on my recent post about some recent work on the intersection of stem cells and human evolution. I noticed that several people expressed variations on the same theme, one which deserves a response. To recap briefly: a great deal of research indicates that a couple million years ago, our hominid ancestors lost the ability to make one of the main sugars that coat mammal cells, called Neu5Gc. This ancient chapter in our history turns out to have a big effect on current research on embryonic stem cells. When human stem cells are raised on a substrate made of mouse cells or calf serum, they absorb the nonhuman Neu5Gc sugars, which ends up on their surface. Humans carry antibodies to Neu5Gc, and these antibodies attack stem cells raised on animal substrates. As a result, existing cell lines fed on this stuff would likely be destroyed if they were implanted in a person.

Some readers questioned whether the research I discussed actually supported evolution and not creationism.

Samuel asked: "If humans are missing this sugar, and the rest of the animal kingdom has it, wouldn't that make humans unique? Could this evidence also support the creationist theory?"

In a similar vein, Graham Mitchell emailed me, writing, "I do find it interesting that you detail how the loss of this sugar in hominids occurred maybe three million years ago and that most other mammals (including primates) still have the sugar, but yet you interpret this evidence as making Intelligent Design *less* likely. As I was reading along, I thought to myself, 'Wow, more evidence that a Designer created humans to be distinct from the animals.'"

I'm happy to respond to these messages, but it's tricky. Neither what Samuel calls "the creationist theory" or what Graham calls "Intelligent Design" offers an explicit hypothesis about how this aspect of our biology came to be. Was mankind created 6,000 years ago without Neu5Gc? Or did a Designer (I'll use Graham's capital D) shut down Neu5Gc 2.5 million years ago in hominid ancestors of humans, with the intent of creating a special species? This is the sort of vagueness that leaves practicing biologists cold when it comes to creationism.

The main point Samuel and Graham are making is that the lack of Neu5Gc appears to be the work of a Designer/Creator who made humans unique from animals. But the lack of Neu5Gc does not actually make us unique. Note that in my original post, I did not say that Neu5Gc is found "in the rest of the animal kingdom," as Samuel put it. I said it was found on every mammal except humans. That's an important difference. The vast majority of animal species--not mention the millions of species of fungi, plants, and bacteria--do not have Neu5Gc. What's more, we have a related sugar called Neu5Ac which all mammals do, and which non-mammals orgnaisms do not.

So our lack of Neu5Gc cannot be interpreted as an example of how the Designer made us unique. On the other hand, there's an obvious (and testable) hypothesis about this evidence that emerges from the theory of evolution. Namely, Neu5Gc and Neu5Ac evolved in the ancestors of living mammals--probably from a similar sugar that can be found on the cells of non-mammals. Then in the human lineage, one of those sugars--Neu5Gc--was lost due to a mutation.

Mind you, evolutionary biologists do not contend that humans are not unique--in the sense that you can scan the human genome and find stretches of DNA not found in any other species. But being unique is not all that...well, not all that unique. A sea slug is also unique, because it also has stretches of DNA not found in any other species. But we would be surprised to hear a sea slug declare that its genetic makeup is evidence that a Designer created it to be distinct from the animals (and not merely because sea slugs are a pretty quiet bunch).

In fact, the study of evolution very much concerned with how humans--and other species--became unique. Evolutionary biologists look at the biology we see around us today and aim to infer how those processes could have produced the diversity of life that surrounds us (and includes us). Some aspects of the history of life are harder than others to study, because there's less evidence at hand. But in the case of Neu5Gc, some things are nicely clear. The gene that makes Neu5Gc in other mammals is not missing from our genomes. It's still sitting there. But right in the middle of it is a distinctive sequence of DNA that belongs to a sort that geneticists understand quite well, called an Alu element.

Alu elements get copied by our cells and those copies get inserted all over our genomes. Scientists can watch the process up close by putting molecular tags on Alu elements in a colony of cells, and then watching it spread over time. In the real world, a fertilized egg may wind up with a new Alu element, which then gets spread to every cell in the baby's body. Out of every 200 births, one child is born with a new Alu element. Sometimes they wind up wedged in the middle of a gene, disrupting its ability to make a protein. In some cases, this leads to a disease. More often, though, the new Alu element ends up somewhere in the genome where it doesn't do much harm. As a result, Alu elements piled up in the ancestors of living humans. The human genome has 1.2 million Alu elements, making up about 10% of its entire sequence of DNA.

Alu elements all work the same way, and all have the same basic genetic sequence. But they are not identical. That's because each time an Alu element gets copied, there's a chance the copying machinery of our cells will make a mistake and introduce a mutation. So Alu elements can be grouped together into families, related by common descent, which in turn can be related to other Alu families. Humans have some unique Alu elements that emerged after we split from other apes, and we also have Alu elements that we inherited from our common ancestor with other apes.

The gene that makes Neu5Gc is interrupted by an Alu element. It's the same Alu element in the same place in the same gene in every person every studied. Scientists can document Alu elements interrupting genes today, either in laboratory experiments or in the maternity ward.

How do we explain this pattern?

On the one hand, there's evolution. The basic idea behind evolution is that mutations have continuously emerged in DNA, leading to variations between individuals in a population. Some of these variations may give individuals an edge in reproducing. If those variations can be inherited, they will gradually become more common. Some populations may split off from the other members of their species and become a new species of their own, but they still carry the adaptive mutations from their common ancestors. And over very long periods of time, many mutations can arise leading to new complex traits.

The case of Neu5Gc is completely consistent with evolution. Scientists may not yet understand what advantage the mutation that robbed us of this sugar had, but the fact that our knowledge is incomplete is not a compelling argument against evolution. After all, scientists don't even know what Neu5Gc andNeu5Ac do today. That doesn't mean the sugars don't exist, or that they aren't important. (As I mentioned before, if you take away these sugars from a mouse through genetic engineering, you end up with a dead mouse.)

Is all of the evidence I've presented consistent with "creationist theory" or "Intelligent Design"? Perhaps someone can offer an explanation that can make it fit, but I don't see it. To create this part of our genome, the Designer would have had to have inserted an Alu element by hand at a particular place in our distant ancestor's genome in order to produce this change. And if Intelligent Design really is supposed to be a scientific theory, that would mean that every time an Alu element winds up somewhere else in the genome, it's the work of a Designer. (You can't just pick and choose the cases that the Designer is responsible for.) And that means that every time someone dies of an Alu-related cancer or other disorder, it's because the Designer invisibly slipped into the body of his or her parents and monkeyed with an egg or a sperm to make sure they died. I look forward to reading the scientific paper documenting that.

Last October, word leaked out that something might be seriously amiss with the embryonic stem cell lines approved by President Bush for federally funded research. Today, the full details were published on line in Nature Medicine. It's an important paper, and not only because it points out a grave problem with the current state of stem cell research. It also shows how scientists who do cutting-edge medical research are looking back at two million years of human evolution to make sense of their work. At a time when antievolutionists are trying hard to wedge creationist nonsense into science classrooms, this is something worth bearing in mind.

This new research focuses on the sugar molecules that coat our cells like frosting on a cake. Two of these sugars are common on virutally every mammal. They are abbreviated as Neu5Ac and Neu5Gc. These sugars are clearly essential to survival. When scientists altered the genes of mice so that they couldn't produce them, the mice died. The sugars probably have several vital roles. They probably work as identity badges, judging from the fact that mammal cells also have receptors that can lock onto these particular sugars and only these particular sugars. Cells need to recognize each other for many reasons, such as when they are developing together to form a complex organ like a liver or a brain.

A surprise was in store for scientists who began looking for these two sugars in the human body. They found plenty of Neu5Ac, but they found practically no Neu5Gc. This is no minor difference, abbreviations aside. Neu5Gc is very common in other mammals. In gorillas, our close relatives, it makes up between 20% to 90% of this group of sugars. In us, zip. We are unique, in fact, among mammals for lacking this molecule.

Ajit Varki of UCSD led the research that established that Neu5GC is missing from humans. He decided to figure out how it disappeared. Other mammals make Neu5Gc by tinkering with Neu5Ac. The enzyme that does the actual tinkering is known as CMAH. This enzyme is pretty much identical in mammals ranging from chimpanzees to pigs. In humans, Varki and his colleagues discovered, the gene for CMAH is broken. It produces a stunted version of the enzyme which can't manufacture Neu5Gc, and so our cells end up with none of these sugars on their surfaces.

The CMAH gene is broken the same way in every person that has been studied. That strongly suggests that all living humans inherited the mutation from a common ancestor. Since chimpanzees, our closest living relatives, have a working version of the gene, that ancestor must have lived less than six million years ago. Scientists can even say exactly how the gene mutated. A parasitic stretch of DNA known as an Alu element produced a copy of itself which got randomly inserted in the middle of the CMAH gene.

But Varki didn't stop here. He joined with experts on extracting ancient biomolecules from fossils. They ground up bits of bones of Neanderthals, which split off from the ancestors of living humans about 500,000 years ago. In 2002 they reported that they found Neanderthal Neu5Ac, but no Neu5Gc. Neanderthals probably inherited the same mutation as we carry. Thus, the mutation must have struck hominids before 500,000 years ago.

To narrow their estimate further, the researchers looked closely at the Alu element that had caused the mutation. They compared its sequence to the original version from which it had been copied. They also looked at related versions in other primates. Studies have shown that this parasitic DNA mutates at a relatively steady rate. So by comparing the mutations in the different versions, they could estimate how old the sugar-disrupting mutation was. They came up with 2.7 million years ago, plus or minus 1.1 million years. While this estimate spans a couple million years, it still falls nicely between the range suggested by earlier research.

This study was the first to pinpoint a mutation that produced a signficant biological change in the hominid lineage. Just three years later, we have hundreds to choose from. But the loss of Neu5Gc still remains an important discovery because it is a loss. As I wrote in an earlier post, losing genes may actually be as important to human evolution as gaining new ones. Losing genes can sometimes release us from restraints that prevented our ancestors from exploring new ways of living. Exactly what advantage giving up Neu5Gc provided isn't clear, according to Varki, but he has some suspicions. Parasites have evolved receptors that can grab onto both sugars, an important step in invading a cell. It's possible that losing one of these sugars helped our ancestors become more resistant to some disease.

Varki also points out that the elimination of Neu5Gc might have been particularly important for the hominid brain--which, perhaps not coincidentally--went through a huge expansion roughly around the time that the Neu5Ac mutation occurred. In other animals, Neu5Gc is abundant on the cells of most organs, but exceedingly rare in the brain. It is very peculiar for a gene to be silenced in the brain, which suggests that it might have some sort of harmful effect. Once a mutation knocked out the gene altogether, hominids didn't have to suffer with any Neu5Gc in the brain at all. Perhaps Neu5Gc limited brain expansion in other mammals, but once it was gone from our ancestors, our brains exploded.

This is not merely a just-so story. In Varki's lab, researchers are breeding mice that can't produce Neu5Gc and others that make too much. If Varki is right, the alter mice should wind up with altered brains.

Now for the stem cells.

Varki has been puzzled by the fact that some scientists over the years have reported detecting tiny amounts of Neu5Gc in humans. If, as Varki has found, the genetic machinery for making this sugar is broken beyond repair, how are they getting it? He and his researchers have spent several years attacking the problem. Their experiiments indicate that we pick up the sugars from the foods we eat--in particular beef and other meat from mammals. Our cells absorb the foreign Neu5Gc and stick them on their surfaces, alongside their normal Neu5Ac sugars. It's possible that their similarity fools our cells into making this mistake. This happens only rarely, but often enough that we develop antibodies to Neu5Gc. In other words, our bodies know that Neu5Gc is the enemy.

It occurred to Varki that something similar might be happening in the production of embryonic stem cells. Once these cells are taken from an embryo, scientists traditionally lay them on top of a layer of mouse embryo cells and calf serum, which provide a supply of food for them. This food, it turns out, is loaded with Neu5Gc, and Varki--working with Fred Gage of the Salk Institute--discovered that it ends up on the human stem cells like frosting on a cake. And Varki and Gage found that human antibodies against Neu5Gc readily attack the stem cells.

If these stem cells were put in people, they might well be destroyed by antibodies. And even if they weren't, the foreign Neu5Gc on their surfaces could cause problems. Both Neu5Gc and the normal Neu5Ac help cells recognize each other, which is crucial during development, when cells stick together to form new structures. Confused cells could wind up producing developmental defects.

Now I suppose that opponents of embryonic stem cell research might seize on this research. Most of the embyronic stem cell lines now being studied could never be implanted in people to provide a new supply of neurons or heart tissue, because they'd be attacked as foreign tissue--exactly the sort of trouble that stem cells were supposed to avoid. Better to scrap the whole line of research and just focus on adult stem cells. (This article in Forbes seems to push this line.)

But this doesn't really make sense on strictly scientific grounds. Scientists could just scrap their existing lines of stem cells and start new ones, making sure that they can't take up Neu5Gc. This would be a challenge, but not an impossible one. Varki and Gage suggest feeding stem cells on serum taken from the person who is going to receive them, for example. Since we really don't know whether embryonic or adult stem cells are going to work as cures, why should scientists simply walk away from embryonic stem cells in the face of a challenge?

The irony is that scientists who rely on federal funding have no choice but to walk away. Starting a new stem cell line is expressly verboten under Bush's decree, because it crosses the moral line he has drawn in the sand. Varki and Gage's results will spell certain doom for embryonic stem cell research only if the government wants it to.

I have noticed that members of the Discovery Institute, the headquarters for lobbying for Intelligent Design, are also speaking out against embryonic stem cell research. It will be interesting to see if they try to embrace Gage and Varki's research while still trying to cast doubt on evolution. How on Earth, I wonder, could someone promoting Intellgent Design or Young Earth creationism make sense of these scientific results? How could they explain away so many facts that line up to present us with an evolutionary history taking us down through millions of years, from our common ancestor with other apes, to the first hominids to evolve large brains, to the rise of Neanderthals and our own species, to the latest breakthroughs in medicine? I do try to imagine how they would do this from time to time, but without much luck. I think I'll keep track of real science instead.

Update, Monday January 24, 2005: The paper is not on the Nature Medicine site yet. I will post a good link as soon as one becomes available.

Update, Monday, 3:00 pm: Welcome, citizens of Slashdot and Metafilter. There sure are a lot of you!

Nature Medicine has made the PDF of the Varki paper available for free on their home page. (Scroll all the way down.)

Update, Friday, 5 pm: Here's a follow-up post on why I don't think this proves the handiwork of an Intelligent Designer.

The Guardian has a long but disjointed report about the dispute over Homo floresiensis. Articles like these rarely give a very good picture of scientific disputes, since all parties involved only get a couple catchy quotes apiece. I've been particularly puzzled by Teuku Jacob, the elderly Indonesian paleoanthropologist who sparked the controversy by taking possession of the bones and locking them away from the Indonesian and Australian researchers who found them. So I was pleased when my brother, a linguistic anthropologist who does research in Indonesia, passed on this link to a translation of a long essay by Jacob. My brother promises me that the translation is accurate. There's a fair bit of science here, although Jacob isn't averse to calling his Australian rivals "latter-day conquistadors."

The more time I spend talking to biologists, the more they remind me of detectives. I have two stories in tomorrow's New York Times that make this connection particularly clear. In the first, E.O. Wilson attempts to solve the mystery of a plague of ants that devastated some of the earliest Spanish settlements in the New World. In the second, I look at another mystery--is there life on Saturn's moon Titan. The space probe Huygens will be falling into its hazy atmosphere on Friday to see what lurks under its cloak. I inteviewed University of Florida chemist Steven Benner who will be trying to search for signs of life in Huygens's data. But if Titan does have life, it may not be based on DNA or even need liquid water. So how do you look for something you've never seen before?

During my interview with Dr. Benner, he said something I found particularly apt about this sort of detective work--but which unfortunately had to be cut for space. “Those of us who do professional science in this area do get a degree of emotional balance. Most of the time science fails. So you meter your emotions.”

Not long ago I had a remarkable experience: I got to visit the nursery for what might prove to be a new form of life. At Michigan State University, a group of computer scientists, biologists, and philosophers run the Digital Evolution Laboratory. There, they are developing software called Avida which allows them to create virtual worlds swarming with digital organisms. Avida's residents show a lot of the important features that scientists consider essential requirements for life. Their evolution is particularly impressive, because it parallels evolution in the wet world in all sorts of subtle ways. And because you can run through a hundred thousand generations in a matter of hours, the Avida team can carry out experiments on some of the most important aspects of evolution that biologists could previously only study by looking at the natural world.

For more details, you can read my cover story in the February issue of Discover.

When you consider a tapeworm or an Ebola virus, it is easy think of them as being evil to their very core. That's a mistake. It's true that at this point in their evolutionary history these species have become well adapted to living inside of other organisms (us), and using our resources to help them reproduce themselves even if we get sick in the process. But one of the big lessons of modern biology is that there are no essences in nature--only the ongoing interplay of natural selection and the conditions in which it works. If the conditions change, organisms may evolve into drastically different things. Even the most ruthless parasite may discover the virtues of peace and harmony--if the conditions are right.

Joel Sachs and James Bull, two biologists at the University of Texas, have offered a vivid demonstration of this fact with the help of bacteria-infecting viruses, called bacteriophages. Bacteriophages, such as the one shown here, are wickedly elegant in the way they find hosts and inject their DNA, which then hijacks the bacteria's cellular machinery to make new bacteriophages. (For more of my praise of the bacteriophage, plus an excellent movie of the beast, go here.)

Bacteriophages fit the definition of parasite to a T. In many cases new viruses multiply inside a host until the bacterium simply rips apart. In other cases, they make bacteria sick, draining resources from their hosts that could otherwise be used for the hosts' own reproduction. But, as Bull and his colleagues have shown in a series of experiments, bacteriophages are not malicious in their very essence. Depending on the conditions in which bacteriophages find themselves, they can evolve into milder forms, or into meaner ones.

Bull and his colleagues took advantage of the fact that many bacteriophages can infect new hosts in one of two ways--by escaping one bacterium to invade another, or by getting passed down from one bacterium to its offspring. These two routes are called horizontal and vertical transmission. Bull's team experimentally created conditions that favored vertical transmission, and within a few dozen generations the viruses became much milder. If you rely on your host's survival for your own survival, it doesn't pay to be a brutal killer. (I wrote more about this evolutionary trade-off--and some of the debate surrounding it--in this article for Science.)

Now Bull and Sachs show that bacteriophages can even evolve to be nice to other bacteriophages. They describe the experiment in the January 11 issue of the Proceedings of the National Academy of Sciences. They started out with two bacteriophages, called f1 and IKe. Both viruses infect E. coli bacteria, but they enter in different ways. f1 only grabs onto one type of hair on the surface of E. coli (the F pilus), while IKe invades its hosts through another type (the N pilus). In the wild, f1 and IKe don't get along well. If they end up in the same host, they compete for the bacterium's cellular machinery. Also, because they are close relatives, sharing the same 10 genes, DNA-binding proteins of one bacteriophage can accidentally grab the DNA of the other species. As a result, bacteria infected with both f1 and IKe produce fewer copies of each virus than bacteria infected with only one species. It's the classic Darwinian scramble.

But Bull and Sachs wondered what would happen if the survival of both bacteriophages actually depended on their coexistence. Here's how they answered the question. First they engineered both bacteriophages, adding a gene that provides resistance to a different antibiotic (kanamycin for IKe and chloramphenicol for f1). Then they dumped billions of the engineered viruses into beakers full of E. coli. They allowed the viruses 16 minutes to find hosts, invade them, and start producing the proteins that confer antibiotic resistance. Then they added the two antibiotics to the beakers. Only the bacteria that had been infected with both bacteriophages could survive the assault. If a bacterium harbored only f1, for example, it would still die, because it remained susceptible to kanamycin.

Next, Bull and Sachs let the bacteriophages and their hosts alone for an hour. The bacteria divided, while the bacteriophages made copies of themselves. After an hour, the scientists dissolved away the bacteria, leaving behind the viruses. These new viruses were then added to a fresh batch of bacteria, and the cycle repeated itself.

Viruses are notoriously sloppy at replicating. The odds of a new virus winding up with a mutation is much higher than for organisms like ourselves, equipped as we are with enzymes that act like genetic proofreaders. As a result, with each round of Bull and Sachs' experiment, many variants emerged in both the f1 and IKe populations. The variants that were best suited for reproducing in the experimental conditions were favored by natural selection, and over time the viruses evolved. After 50 rounds, Bull and Sachs stopped the experiment and took a look at what the bacteriophages had become. Were they so selfish that they had driven themselves extinct? Or had they come to some sort of accommodation?

The bacteriophages clearly went through natural selection during just 50 rounds. By that point f1 was producing 50 times more copies of itself, and IKe was producing 1,000 times more. At the beginning of the experiment sharing a host was a bad thing for these viruses, but at the end it had become a very good thing. Bull and Sachs discovered that they had overcome their conflict of interest in an extraordinary way: they practically merged into a single organism. When Bull and Sachs opened up a bacteriophage shell, very often they found both the f1 and IKe genomes sitting side by side. They cold still find plenty of viruses with a single genome inside, but even in these cases, evolution had taken a dramatic turn. By about round 20, the IKe viruses had lost the ability to make their own protein coat. Instead, they borrowed f1 coats.

Bull and Sachs argue that the bacteriophages adapted to the experiment in a clever way. If you're a bacteriophage, successfully invading a host on your own is not enough to stave off death, because you may find yourself alone. If a mutation lets you bring along the other virus with you, then you are pretty much guaranteed survival. For some reason, f1 seems to have taken the lead in this cooperation, mutating in such a way that IKe genomes could slip easily inside f1's protein coats. As a result, IKe began to lose its own ability to survive as an independent virus, relying instead on the cooperation of f1. Once the viruses were packaged together, they no longer had a conflict of interest, and they could evolve an even greater level of cooperation.

Evolutionary biologists have long been fascinated by cooperation, whether the cooperators are chromosomes in a single cell, individual bacteria in a colony, or people in a village. What keeps individuals from cheating on others, from choosing the selfish strategy rather than the selfless one? Scientists have constructed sophisticated mathematical models in order to find the right sort of conditions where cooperation might evolve. But Bull and Sachs point out that it only took them 50 generations to turn uncooperative bacteriophages into intimate partners. When they sequenced the viruses, they found that f1 had acquired just eight mutations in its DNA, and IKe had acquired nine. Perhaps cooperation is not such a big deal after all. And perhaps parasites are not the essence of evil we tend to believe them to be.

Evolutionary biologists face a challenge that's a lot like a challenge of studying ancient human history: to retrieve vanished connections. The people who live in remote Polynesia presumably didn't sprout from the island soil like trees--they must have come from somewhere. Tracing their connection to ancestors elsewhere hasn't been easy, in part because the islands are surrounded by hundreds of miles of open ocean. It hasn't been impossible though: studies on their culture, language, and DNA all suggest that the Polynesians originally embarked from southeast Asia. We may never be able to retrieve the full flow of history that carried people thousands of miles to the middle of the Pacific, but we can know some things about it, and we can rest assured that some things are definitely not true (such as the sprouting-from-the-ground theory).

Whales are a lot like Polynesians. All living species of whales look a lot like each other, and not very much like any other animals. They all have horizontal tail flukes, blowholes, and smooth skin free of scales or fur. Darwin argued that whales were not simply created in the oceans in their current form, but instead descended from land mammals which had adapted to life in the ocean. He pointed out that whales share a number of traits with land mammals, such as milk and a placenta. Their blowhole connects to a set of lungs very much like those of land mammals and nothing like the gills of fish.

Darwin wigged out more than a few people with this argument. Whales just seemed too different, too distinct to have evolved by small steps from a four-legged ancestor. And creationists loved to point out how unlikely this transition seemed--on par with turning a cow into a shark. They also liked to point out that no intermediate fossils had ever been found. But as I wrote in my book At the Water's Edge, paleontologists began to find those fossils in the 1980s. Today, the transition whales made from land to sea is wonderfully well documented. Paleontologists have found complete skeletons of creatures such as the 45 million year old Ambulocetus (reconstructed here by the gifted artist Carl Buell). The transformation was not some sudden macromutation, but a gradual series of changes over millions of years, featuring shrinking legs, lengthening tails, loosening hips, and migrating noses.

In the coming century, I suspect fossils will help scientists reconstruct other major transitions. But they'll also start reconstructing others that have left no record in rocks A fascinating case in point has been published on line at the Proceedings of the National Academy of Sciences. Jan Klein and Nikolas Nikolaidis of Penn State have drawn a rough map that charts the evolution of the immune system.

Our immune system is as awesome as a whale's body--in terms of the complexity of its parts and the way those parts work together so well. It keeps viruses, bacteria, tapeworms, and even cancer cells at bay, while generally sparing our own tissues from its withering attack. All animals share a rudimentary immune system, but Klein and Nikolaidis focused on a second system that is found only in vertebrates. Only we vertebrates have immune systems that can learn.

This learning system is a network of cells, signals, and poisons. Among its most important cells are T cells and B cells. They originate in the bone marrow, although the T cells have to finish their development in the thymus, an organ near the heart. These cells are unusual in many ways, most important of which are some of the receptors they make on their surface. The cells have a special set of tools that cut up the receptor genes and paste them into new arrangements, so that the genes produce receptors with new shapes. Depending on its shape, a receptor can grab onto certain molecules. Those molecules may come from a bacteria toxin, or they coat nerves or muscle cells. Our bodies can usually eliminate the immune cells that have an affinity for our own tissue. If they don't, we end up with autoimmune diseases such as muscular dystrophy.

The surviving B cells and T cells are introduced to molecules from invading pathogens (antigens) by other immune cells called macrophages. The macrophages devour bacteria or virus-infected cells and then put some of the molecules of their victims on their surface. They travel to the lymph nodes to show off their conquests. If T cells or B cells bump into one of these macrophages, their receptor may fit reasonably well onto an antigen. That fit sends a signal to their DNA, triggering them to multiply. Some of the cells they produce receptors cut and pasted into newer shapes, some of which do an even better job of fitting on the antigen. These winners get to reproduce more. In other words, our immune systems use a version of natural selection to fine tune their recognition of pathogens.

These B cells and T cells can then fight off a disease. The T cells may destroy cells infected with the pathogen, because most cells in the human body have receptors they can use to display antigens. In other cases, they can whip up macrophages into a furious frenzy of killing. Or they may spur B cells to produce antibodies. The B cells spray out the antibodies into our bodies, and when they come into contact with their particular pathogen, they may drill into it, stop it from invading cells, or tag the pathogen to make it an easier target for macrophage attack. Some B cells and T cells that can recognize a pathogen sit out the battle. If we should be exposed to the same disease years later, these memory cells can leap into action so quickly that the new infection may not even make us sick.

You can find this same remarkable system in humans, albatrosses, rattlesnakes, bullfrogs, and all other land vertebrates. You can also find it in most fish, from salmon to hammerhead sharks to sea horses. There are some variations from species to species, but they've all got B cells, T cells, antibodies, thymuses, and the other essential components. But you won't find it in beetles, earthworms, dragonflies, or any other invertebrate on land. Nor will you find it in starfish, squid, lobsters, or lampreys in the water. All these other animals rely instead on rudimentary immune systems that cannot learn.

For those who reject evolution, this sort of pattern tells them nothing. Like everything else in nature, they can only wave their hands and declare it the inscrutable work of a designer (lower case d or upper case D as they are so inclined on a given day). But immunologists and other scientists who actually want to learn something about the immune system find this view useless. Instead, they look at how animals with an antibody-based immune system are related to one another. And what they find is both straightforward and astonishing. All of the living animals with an antibody-based immune system descend from a common ancestor, and none of the descendants of that common ancestor lack it. That means that the antibody-based immune system evolved once, about 470 million years ago.

I need to back up in the history of life a few hundred million years to explain how scientists know this. Studies on fossils and genes agree that everything we call an animal (including sponges and jellyfish) shares a common ancestor not shared by plants, fungi, or other major groups of organisms. Exactly when that ancestor lived is a subject of fierce debate, but one of the latest estimates puts the date at about 650 million years ago. This ancestor probably had a simple immune system, because all animals, from sponges on, have at least some sort of defense against pathogens. Over the next 100 million years or so, the major groups of animals branched off from one another, and while some branches evolved some new defenses of their own, the antibody-based immune system only appears in our own branch, the vertebrates.

Animals with some--but not all--of the key traits of vertebrates, such as heads and brains, lived at least 530 million years ago. The only living relics of these early branches are hagfish. Later, our ancestors also evolved a vertebral column, becoming true vertebrates. Lampreys represent the deepest branch of vertebrate evolution, splitting off perhaps 500 million years ago from their common ancestor with us. They lack many traits that other vertebrates have--most obviously a jaw. A number of other weird jawless vertebrates filled the oceans between about 500 and 360 million years ago, but except for lampreys, they're all long gone. One of these branches gave rise over 470 million years ago to fish with jaws--known as gnathostomes. Gnathostomes later gave rise to sharks and other "cartilaginous" fishes, as well as ray-finned fishes, and land vertebrates.

You may have already guessed the kicker of all this history. Lampreys and invertebrates don't have an antibody-based immune system. Sharks, ray-finned fish, and land vertebrates do. Sharks, ray-finned fishes, and land vertebrates all share a common ancestor that is not shared by lampreys or other invertebrates. The simplest way to explain this coincidence is to conclude that the antibody-based immune system evolved after lampreys branched off from our own lineage, but before sharks and other living gnathostomes began to branch apart. We can't dig up fossil antibodies, but we can know when they evolved.

Scientists have sometimes treated the transition from rudimentary immune system to antibody-based immune system as a great leap. Lampreys don't have antibodies, B cells, T cells, thymuses, or the rest, and all gnathostomes do. Some creationists have even tried to turn this into an argument against evolution, claiming that something as complex as the adaptive immune system could not have emerged gradually. But it's important to bear in mind that tens of millions of years of evolution separate our common ancestor with lampreys and the earliest gnathostomes. And in their new paper, Klein and Nikolaidis argue that the evolution of the antibody-based immune system was a lot like the evolution of whales: a gradual, step-wise process.

Most of the components of the antibody-based immune system were actually already in place long before gnathostomes evolved. Lampreys, for example, don't have a thymus, but they do have the structures and cell types that form the thymus. In gnathostomes, the thymus develops as cells switch on special genes in a particular order. Lampreys have these genes, as so many other animals. Instead of building thymuses, they build other structures, such as eyes and gill arches. It would have only required altering the switches that determine when and where these genes become active to produce a new organ.

B cells and T cells are known as lymphocytes. Lampreys don't have lymphocytes, but Klein and Nikolaidis point out that they do have "lymphocyte-like cells." (The picture above shows what these cells look like.) Lymphocyte-like cells develop like lymphocytes, under the control of many of the same genes that control the development of lymphocytes. Once they are mature, these cells have almost the same structure and chemistry as lymphocytes--but they don't produce the antibodies and receptors of B cells and T cells. Exactly what they do in lampreys isn't clear.

What about those receptors and antibodies? Klein and Nikolaidis point out that they aren't quite as novel as they may look at first. They are made up of building-blocks of simple proteins arranged in different ways. And guess what--many of these simpler proteins are found in lampreys and invertebrates, where they serve other functions. The same goes for many of the proteins that B cells and T cells use to communicate with one another. Other proteins are made by genes that are unique to gnathostomes, but show a kinship to entire families of genes found in other animals. The most likely explanation is that an ancestral gene duplicated by accident, and later one of the copies was recruited to the evolving immune system.

Klein and Nikolaidis point out that some truly new things appeared as the antibody-based immune system emerged. But just because something is new doesn't mean that it couldn't have evolved. The best-understood example of a new feature is the cut-and-paste machinery that allows B cells and T cells to mix up their receptors into new shapes. Scientists have been working out its evolution for years now, but just last week some scientists from Johns Hopkins published a paper in Naturethat brought the picture into remarkable focus. Our genomes are rife with virus-like sequences known as transposable elements that produce enzymes whose sole function is to make copies of the transposable DNA and insert those copies somewhere else in our genomes. In a few cases, these transposable elements have evolved from pests to helpers, carrying out important functions in our cells. The genes that are responsible for cutting and pasting immune cell receptors bear a clear resemblance to transposable elements in other animals. So the evolution of a new cut-and-paste mechanism was actually just the domestication of an in-house virus.

I suppose that creationists might claim that these components could not possibly have come together into an antibody-based immune system. But there's no proof behind this sort of categorical dismissal, just a personal feeling of disbelief. These folks would still be left with the fact that the evolutionary tree of life and the biochemistry of vertebrates and other animals are all consistent with a gradual evolution of this system. It would all have to be a spectacular coincidence, or perhaps an intentional deception on the part of the designer. Who knows. Who cares, really? (Aside from certain Pennsylvania senators.) What's exciting here is the future research that could shed more light on this transition. Klein and Nikolaidis propose introducing lamprey genes into vertebrates and vice versa to see just how close the ancestors of lampreys had gotten to an antibody-based immune system before they branched off on their own. Obviously, some half a billion years of independent evolution will muddy up the results, but it should be possible to see whether gnathostome immune genes can organize the lamprey immune system to act more like our own. What I'd be even more excited by would be a deep-sea discovery of a living fossil--a jawless fish that is more closely related to us than lampreys. They filled the seas 400 million years ago, and perhaps a few are lurking in some deep sea trench. Such a fish might have a crude antibody-based immune system, with only a few genes recruited and others yet to be pulled in. Perhaps it could do a mediocre job of learning to recognize diseases--but a mediocre job is better than no job at all.

It may sound like a crazy dream, but then again, so did walking whales.

Size matters. At least that's the result of some recent research on long-term evolutionary trends that I'll be reporting in tomorrow's New York Times. Here are the first few paragraphs...

Bigger is better, the saying goes, and in the case of evolution, the saying is apparently right.

The notion that natural selection can create long-term trends toward large size first emerged about a century ago, but it fell out of favor in recent decades. Now researchers have taken a fresh look at the question with new methods, and some argue that these trends are real.

Biologists have recently found that in a vast majority of animals and plants, bigger individuals are more successful at reproducing than smaller ones, whether they are finches, damselflies or jimsonweed.

Nor is this edge a fleeting one. Natural selection can steadily drive lineages to bigger sizes for vast stretches of time. The giant dinosaurs that made the earth tremble, for example, were the product of the long-running advantage of being big over tens of millions of years.

"I think it holds up very well, and a lot better than a lot of people have said over the years," said David Hone, a paleontologist at the University of Bristol. Mr. Hone and others argue the push toward bigger size is so strong and persistent that there must be significant forces pushing the other way. Otherwise, we would be living on a planet of giants.

You can read the rest of the article here.

As is so often the case, I wish the article could have ended with a big fat asterisk, along with a footnote reading, "There's more to the story, but you'll have to visit The Loom for it."

This notion about size increase, known as Cope's Rule, has a long, checkered history, and this history say a lot about how the entire science of evolutionary biology has changed over the years. Cope's Rule is named after the American paleontologist Edward Drinker Cope, who made a careful study of the fossils of North America in the late 1800s. Cope belonged to the first generation of scientists who grappled with Darwin's Origin of Species, published in 1859. Its reception was decidedly mixed. On the one hand, Darwin was hugely successful in persuading scientists that life had evolved over a long period of time, thanks to the huge amount of evidence he marshalled fossils, embryos, and the distribution of living species. But Darwin didn't fare so well in his argument about what drove the evolution of life. He was trying to quash the popular ideas of Lamarck, who had offered two mechanisms for evolution. First, traits acquired over an individual's lifetime are passed on to its descendants. Second, life contains a mysterious force that continually drives it from lowly primordial slime towards higher levels. Darwin rejected both of these mechanisms almost completely, replacing them with natural selection.

This second argument did not fare as well in the late 1800s as the first. Many biologists came to see life as the product of evolution, but they saw evolution as the product of various Lamarckian, long-term forces. Cope was one of these scientists. He looked at the early mammals of North America--tiny creatures, for the most part--and saw that later they were replaced by much larger species. Here, he decided, was evidence of an evolutionary force that could operate over millions of years, a force, moreover that was separate from natural selection. Others found similar patterns in other groups, such as corals and foraminfera.

In the mid-twentieth century, evolutionary biology went through a revolution known as the Modern Synthesis. Scientists came to understand how genes mutate, and how mutations helped make natural selection possible. Leftover Lamarckism found no vindication of its own, and faded away. Biologists still accepted Cope's Rule as a genuine pattern in the fossil record, but they offered a different mechanism than Cope originally had. Instead of some mysterious long-term trend, good old natural selection was at work. Bigger individuals were favored in populations, and over millions of years, this edge produced bigger and bigger species.

In the 1970s, a group of young paleontologists challenged some aspects of the Modern Synthesis. They rejected the idea that every long-term pattern in the fossil record could be neatly explained by short-term natural selection. And Cope's Rule became one of their favorite targets. A trend towards bigger sizes could appear in the fossil record, they pointed out, even if natural selection didn't favor bigger individuals. Small species, for example, might be more likely to survive mass extinctions, and would thus have been more likely to found major new groups of species. Because they were small, their descendants couldn't get much smaller before they hit a minimum size limit. But they'd have plenty of room at the larger end of the spectrum. Even without an inherent advantage to being big, the lineage would gradually get larger.

Although a number of paleontologists were involved in this rebellion, Stephen Jay Gould was its most outspoken member. He made Cope's Rule a favorite object of his derision, a case study of how our subjective biases ("bigger is better") shape our interpretation of the natural world. And from the 1970s to the 1990s, he had pretty good reason to be scornful. The evidence for Cope's Rule turned out not to be all that strong. Or to put it more precisely, scientists who promoted Cope's Rule did not test it rigorously against other possible explanations.

My article looks at some recent research that gives it the careful look it demands. And, in something of a surprise, Cope's Rule is enjoying a renaissance. In most living populations of animals and plants studied so far, natural selection shows a strong preference for larger size. In rigorous studies of the fossil record, lineages of dinosaurs and mammals show signs of having evolved to bigger sizes over millions of years thanks to natural selection.

So was Gould wrong? Yes and no. Cope's Rule is not, as he claimed, a "psychological artefact." But there must be more to the story than natural selection favoring bigger indvidiuals. Otherwise, we'd live on a planet of giants. In my article, I mention a few possible forces that work against Cope's Rule. One that I didn't have space to mention is a force near and dear to Gould's heart: species selection. Just as individuals are favored or disfavored by natural selection, species may also undergo a selection of their own, with some species giving rise to more descendant species, while others go extinct. In the case of size, what's good for the individual may not be so good for the species.

Species selection has been kicked around for quite some time to explain why Cope's Rule hasn't made everything enormous. Recently, a nice study of fossils came out that supported the idea. Paleontologist Blaire Van Valkenburgh of UCLA and her colleauges have documented how big size may have doomed two groups of canids-the ancient relatives of today's dogs and wolves-in North America. In both cases, the canids evolved to larger sizes over millions of years, only to dwindle away to extinction.

As Van Valkenburgh and her colleagues pointed out in Science in October, small canids could have found enough energy in rabbit-sized prey and other foods such as fruits. But once the canids got above about forty pounds, they could no longer survive on this fare. They would spend more energy running after prey than they got eating them. As the canids got bigger, Van Valkenburgh argues, they shifted to hunting prey as big as themselves or bigger. Consistent with this hypothesis, Van Valkenburgh has found that as both groups of canids got large, their jaws and teeth also evolved. They lost molars, their front teeth got larger, and their jaws became stout and strong. This shift put these canids in an evolutionary trap. If their large prey became extinct, they risked starving to death. Nor could they re-evolve the versatile teeth and jaws that had allowed their ancestors to eat different sorts of food. They didn't go extinct because they were big; they went extinct because they were specialized.

Scientists I spoke to for this article were confident that Cope's Rule would figure in a lot of research in coming years. They've now got the tools they need to dissect long-term trends like never before--from databases of fossils to detailed evolutionary trees to sophisticated statistical methods. After more than a century, Cope's Rule still has plenty of life in it yet.

Intelligence is no different than feathers or tentacles or petals. It's a biological trait with both costs and benefits. It costs energy (the calories we use to build and run our brains) which we could otherwise use to keep our bodies warm, to build extra muscle, to ward off diseases. It's also possible for the genes that enhance one trait, such as intelligence, to interfere with another one, or even cause diseases. Over the course of evolutionary time, a trait can vanish from a population if its cost is too high.

On the other hand, intelligence may offer some evolutionary benefits, by allowing us to find food, withstand the elements, locate the car keys our children have put in their dollhouses, etc. But it is by no means a given that intelligence is always a net plus. It all depends on the conditions in which we--and other animals--find ourselves in.

Scientists have come to appreciate how optional intelligence is through several sorts of experiments. Last year French scientists reported an experiment in which they bred fruit flies for their ability to learn. They would give the flies oranges and pineapples on which to lay their eggs, but they would dab one kind of fruit with a nasty tasting chemical. Some of the flies learned quickly to avoid the bad-tasting fruits, avoiding them even when the researchers didn't put the chemicals on them. These smarter flies were allowed to reproduce, passing on their learning genes to the next generation. (The researchers switched the bad taste between the fruits in each generation to make sure that the flies weren't simply evolving a distaste for oranges or pineapples.) This line of flies became significantly better at learning than their unevolved cousins in a few dozen generations. And in a reverse experiment, they succeeded in breeding stupid flies who did worse at learning than normal flies.

If it was so easy for the scientists to produce better learning in flies, why hadn't the ancestors of these insects already evolved this sort of intelligence in the wild? The answer is that this intelligence comes at a cost. The researchers put the larvae of the smart flies alongside some normal fly larvae and let them compete for a supply of yeast. They then counted how many of the larvae survived to adulthood. Then they did the same experiment with the dumb flies. They found that the larvae of smart flies are more likely to die off than the dumb ones.

Now comes another experiment in intelligence, this one conducted mainly by nature rather than scientists. Many of the streams that feed the Panama canal are inhabited by the same species of guppy, Brachyraphis episcopi. And in many of these streams, the guppies live in two different habitats: above and below waterfalls. Below the waterfalls, they face a lot of competition from other fish that are trying to eat the fruit and other foods that fall from the trees overhead, and they also have to cope with several predatory fish. But above the waterfalls the guppies enjoy a predator free existence. Researchers at the University of Edinburgh realized that this arrangement created excellent conditions for the evolution of different kinds of behavior within a species. Upstream guppies would not face the same evolutionary pressures that the downstream fish were. And if the researchers were right, they should find the pattern repeated in stream after stream.

The researchers netted guppies from four different streams, both from upstream and downstream populations. They then shipped the fish back to their lab in Scotland and tested their ability to make their way through mazes to find food. As they report in a paper in press at Behavioral Ecology, the fish from the low-predator upstream sites consistently outperformed their downstream counterparts. They figured out the mazes twice as quickly.

The researchers argue that the upstream fish do so well because they have been able to evolve a sort of single-mindedness. In the wild, the guppies appear to size up their stream and figure out the best place to wait for food to drop to the water. They head for that patch quickly and defend it from other guppies. This sort of learning translates well into a laboratory maze. The downstream guppies, on the other hand, would risk becoming easy prey if all they did were to search for the best patch of stream. Instead, they also have to get a better sense of their overall habitat, spotting predators, finding refuges, and so on. In the laboratory, they tended to explore more of the passageways of the maze than the upstream guppies, perhaps due to their instinct to get a lay of the land (or perhaps the lay of the water).

These results raise a sticky point about ourselves. They suggest that different populations of the same species (such as humans) can evolve differences in cognition in response to different environments. I don't think these results can be used to boost any notion of race-based difference in IQ, though, because we're not fish or laboratory fruit flies. I don't think the conditions that people in different parts of the world face are as different as these flies and guppies have faced. The most important lesson from these results, I think, is make us tone down our self-love a bit. Being intelligent does not make us superior to other animals. It only makes us superior in one respect.

Imagine you're a columnist. You decide to write something about how the National Park Service is allowing a creationist book to be sold in their Grand Canyon stores, over the protests of its own geologists, who point out that NPS has a mandate to promote sound science. Hawking a book that claims that the Grand Canyon was carved by Noah's Flood a few thousand years ago is the polar opposite of this mandate. So what do you write? Well, if you're Republican consultant Jay Bryant, and you're writing for the conservative web site Town Hall, you declare that this as a clear-cut case of Darwinist atheists censoring freedom of speech in a desperate attempt to squelch Intelligent Design.

I don't blog much about science and politics, because I don't have the time and because others do it better than I could (see Chris Mooney and Prometheus for starters). But there's something so simple and basic about the Grand Canyon affair--with plain scientific fact on one side and eye-popping rhetorical nonsense on the other--that I can't help but register disbelief at it from time to time.

The Australian media are doing a fantastic job of keeping up with the developments with Homo floresiensis. Here's the first three-dimensional reconstruction I've seen of the little hominid, made by an Australian archaeologist. It's published on the Australian Broadcasting Corporation's web site. I'm sure that as more bones emerge, the image will improve, but this is still a wonderful first look.

Homo floresiensis update: The Economist weighs in on the "borrowing" of the fossils. They mention that when the bones were removed, they were simply stuffed in a leather bag. This is not exactly the sort of procedure you see in protocols for avoiding contamination of ancient DNA. In the Australian, the discoverers of "Florence" vow to return to the fossil site, and this time they'll put their discoveries in a really good safe. Wise move.

In tomorrow's New York Times, I have an article about how to reconstruct a genome that's been gone for 80 million years. The genome in question belongs to the common ancestor of humans and many other mammals (fancy name: Boreoeutheria). In a paper in this month's Genome Research, scientists compared the same chunk of DNA in 19 species of mammals. (The chunk is 1.1 million base pairs long and includes ten genes and a lot of junk.) The researchers could work their way backwards to the ancestral genetic chunk, and then showed they could be 98.5% certain of the accuracy of the reconstruction.

There are some pretty astonishing implications of this work. For one thing, it should be possible to synthesize this chunk of DNA and put it in a lab animal to see how it worked in our ancestor. For another, the scientists are now confident that they will be able to use the same technique to reconstruct the entire genome in the next few years, if the sequencing of mammal genomes continues apace. Could scientists some day clone a primordial Boreoeutherian? It's not impossible.

On the down side, this method will not work for just any group of animals you want to pick. Mammal evolution was rather peculiar 80 million years ago: a lot of branches sprouted off in different directions in a geologically short period of time. That makes the 19 species the scientists studied like 19 different fuzzy images of the same picture. Other groups of species had a very different evolutionary history, and one that may make genome reconstruction impossible. If you yearn for the day when Jurassic Park becomes real, you will have to conect yourself with a swarm of shrew-like critters. If they did somehow manage to break out of a lab, I suspect they would get eaten by the first cat to cross their path.

I have a short piece in today's New York Times about how male swallows are evolving longer tails, which female swallows find sexy. Here's the original paper in press at The Journal of Evolutionary Biology. Measuring the effects of natural selection is tough work, the details of which are impossible to squeeze into a brief news article. Scientists have to document a change in a population of animals--the length of feathers, for example--but then they have to determine that the change is a product of genetic change. We are much taller than people 200 years ago, but it's clear that most, if not all, of this change is simply a response of our bodies to better food and medicine. The authors of the swallow paper carried out a number of studies that suggest that the length of swallow tails is genetically based, and that those genes are changing. If they're right--and other experts I contacted think they are--it's a striking example of how quickly the sex lives of wild animals can evolve.

Things get a little fuzzier when the researchers propose what's driving the evolution. They think desertification in the springtime range of the swallows in Algeria is to blame. But it's very hard to eliminate other possibilities, since these swallows have complicated lives, migrating from Europe to South Africa and back every year. It's much easier to make a case for the forces driving the evolution of Darwin's finches, which generally sit obediently on the island on which they were born and are subject to cycles of droughts and heavy rains.

But it's a question very much worth investigating. Global warming may well produce ecological changes that could produce just these sorts of rapid evolutionary changes in animals and plants. In some cases, species may be able to adapt quickly enough to their new environment. In other cases, they may lose the race.

On Wednesday I spoke on "The Current," the Canadian Broadcasting Corporation's morning radio show. The hour-long segment focuses on various aspects of evolution, such as the evolution of diseases and the ongoing creationist circus in Georgia. I spoke about how humans are altering the evolution of other species. You can listen to the entire episode here. The audo file is broken up into pieces; part two and part three are the evolution segment.

Last month saw the bombshell report that a tiny species of hominid lived on an Indonesian island 18,000 years ago. Since then there has been a dribbling of follow-up news. Some American paleoanthropologists have expressed skepticism, pointing out that while bones from several small individuals have been found, only one skull has turned up. The skull was the most distinctive part of the skeleton, with a minuscule brain and other features that suggested it was not closely related to our own species. The skeptics suggest that these hominids were actually modern human pygmies, and that the skull came from an individual who suffered a genetic disorder called microcephaly.

In Friday's issue of Science, Michael Balter reports that a prominent Indonesian anthropologist, Teuku Jacob of Gadjah Mada University, thinks Homo floresiensis was a microcephalic. He has taken possession of the fossils to study them, and this has a number of researchers worried. Jacob is known to guard fossils in his vault, and so he may essentially be making it impossible for other researchers to look at them. Balter quotes one of the authors of the original report on the fossils, Peter Brown of the University of New England in Australia, saying, "I doubt that the material will ever be studied again."

This could be staggeringly tragic, because the world is waiting for the other shoe to drop: is there any DNA in the fossils?

The fossils are so young that they might well contain some genetic fragments, and this DNA could quickly resolve the debate over which species the bones belong to. If they belong to human pygmies, their DNA should be more similar to the DNA of Australian aborigines or Southeast Asians than to Europeans or Africans. But if, as Brown and his colleagues suggest, they belong to a species that branched off from an Asian population of Homo erectus, then their DNA should not be particularly close to any living human's genes. Most evidence indicates that Homo erectus in Asia shares a common ancestor with Homo sapiens that lived two million years ago. It might even be possible to compare Homo floresiensis DNA to the fragments of Neanderthal DNA that have come to light in recent years. If Brown is right, then Neanderthal DNA should be more similar to human DNA than that of Homo floresiensis, because Neanderthals and humans share a common ancestor that lived roughly 500,000 years ago--four times younger than the ancestor we share with Homo erectus.

According to an Australian newspaper, Brown and his colleagues have found hair that may belong to H. floresiensis, and which may contain DNA. But if that turns out to be a dead end, the next best hope will be the fossils. And the biggest challenge in finding fossil hominid DNA is contamination. You don't want to accidentally grab DNA from a lab assistant's thumbprint. If the Homo floresiensis goes down a bureaucratic rabbit hole, that challenge could become enormous.

The early evolution of apes is where some of the most interesting developments are emerging. Until the recent discoveries of fossils of Pierolapithecus catalaunicus and other early species, the fossil record from this period of our history was pretty scanty. These new fossils are starting to shed light on some pretty major questions, such as how our upright stance came to be and how our brains got so big. Meanwhile, new genetic work is raising the curtain on the evolution of cognition in these early apes, which set the stage for our subsequent explosion.

Yet for all the excitement a story like can engenders, some of the coverage has been pretty irritating. Certain hoary misconceptions about science have a way of taking hold in the journalistic world and seem to be impossible to dislodge. One of these is the notion that paleoanthropologists are focused on discovering "the missing link," and that only the missing link can tell us anything of real importance about our origins. Just consider Diedtra Henderson's article on MSNBC.com. It includes this rather revealing sentence--

"Coaxed by a reporter to say Pierolapithecus catalaunicus represented a 'missing link,' co-author Meike Kohler demurred. 'I don’t like, very much, to use this word because it is a very old concept.'"

That's right--coaxed. As in, "Come on, professor, just give us a smile and say it's a missing link. It won't kill you, right?"

Henderson is hardly alone. A little googling unearths 59 articles that do their best to call Pierolapithecus a missing link, even if it means putting a question mark after it in a headline. Today, Ira Flatow on Science Friday asked his paleoanthropologist guest whether the fossil is a missing link, even while he acknowledged that the scientist might not want to be "boxed in" with that phrase.

Now, if you learned about human origins 50 years ago, you might well have read things by scientists referring to a missing link in our evolution. The great paleoanthropologist Robert Broom even published a book in 1951 called Finding the Missing Link. But this was a time when so few fossils were known from human evolution that many researchers thought that our ancestry was pretty much linear until you got back to our common ancestor with other living apes. But fifty years later, it's abundantly clear now that human evolution has produced many branches, all but one of which have ended in extinction. Some are close to our own ancestry, others are further away. Paleoanthropologists don't get excited about a fossil because they think they've found the missing link (whatever that is), but because a fossil can show how early a trait such as a big brain evolved, and sometimes can even reveal traits that have evolved independently several times in evolution. That's what gets them fired up about Pierolapithecus catalaunicus. So why shouldn't journalists get fired up as well, rather than trotting out old cliches?

It's not just lazy journalism, I'd argue, but abets some pernicious pseudoarguments made against evolution. Creationists try to cast doubt on the reality of evolution whenever a new fossil of a hominid is discovered. They crow that the latest fossil has a feature not found in living apes or living humans, meaning that it can't bridge the gap between the two groups. These arguments hardly call human evolution into doubt. The only lesson that should be drawn from them is that the term "missing link" should be retired for good.

Apparently so.

...Actually, this new Gallup report shows that 35% of people believe that Darwin's theory of evolution is not supported by the evidence, while another 29% don't know enough to say, and 1% have no opinion. So perhaps I should say, wrong or uninformed.

A little more horn-tooting: The Loom has just been named a winner of the American Association for the Advancement of Science's 2004 Science Journalism Award. The judges considered three pieces: Hamilton's Fall, Why the Cousins Are Gone, and My Darwinian Daughters. Here's the press release. Thanks to the judges--it's gratifying to see that it's possible for a little blog to swim with the big online sharks.

On the other hand, the news is a bit embarrassing, coming as it does while I've left the Loom woefully neglected over the past couple weeks. I've been working on a lot of articles, such as a piece for Science about the new hypothesis that our ancestors evolved to run. (Here's a shorter version; the full version will go online later today.)

Get to know that little skull. Scientists are going to be talking about it for centuries.

As researchers report in tomorrow's issue of Nature, the skull--and along with other parts of a skeleton--turned up in a cave on the Indonesian island of Flores. Several different dating methods gave the same result: the fossil is about 18,000 years old. (Additional bones from the same cave date back to about 38,000 years.) If all you had was the 18,000 year figure and this picture to go on, you might assume that the skull belonged to a small human child. After all, there is plenty of evidence that Homo sapiens had already been in this part of the world for 25, 000 years. But you'd be wrong.

The skull actually belongs to a previously unknown species of hominid, whose ancestors split off from our own some 2 million years ago. Homo floresiensis, as it's known, stood three feet high as an adult and had a brain less than a third the size of our own.

To understand just how mind-blowing Homo floresiensis is, you have to consider it in the context of hominid evolution. Our closest living relatives (chimpanzees and bonobos) live in Africa, and both genetic and fossil evidence indicate that the common ancestor we share with them lived in Africa as well. The oldest known hominids--those species more closely related to us than chimps or other primates--date back 6 million years. They were short, probably could walk upright, and had brains about the size of a chimpanzee--about 350 cubic centimeters. It was only about 2.6 million years ago that hominids started using stone tools, and only about 2 million years ago that species emerged that stood as tall as we do. Its brain was also bigger--850 cc. The increase in brain size may not have been all that significant, since bigger mammals tend to have bigger brains, smart or not. But shortly after this evolutionary surge, the first hominids turned up outside Africa. Homo erectus moved as far east as China and Indonesia within just a few hundred thousand years. At the very least, their migration suggests an expanding population of meat-eaters who have to seek out much bigger ranges than their ancestors.

The Asian population of Homo erectus had little, if anything, to do with our own origins. The oldest human fossils, dating back 160,000 years ago, were found in Africa, and there's a pretty good chain of evidence showing that Homo sapiens descends from hominids who stayed home on the mother continent while Homo erectus swept across Asia. For instance, African hominids underwent a massive burst of brain expansion around 500,000 years ago to close to our own capacity. Meanwhile, Homo erectus in Asia underwent a slight increase, if any. Humans only expanded successfully out of Africa about 50,000 years ago. They may have interbred with Homo erectus, but most of our genome still points back to a recent African origin.

Paleoanthropologists were first attracted to Flores when 800,000 year old tools were found on the island in 1998. Boats seem to have been essential for getting to Flores, which speaks of a pretty impressive mental capacity for Homo erectus . (On the other hand, lizards and elephants and other land animals got to the island without a boat--perhaps by swimming being swept away on logs during storms.) Researchers poked around on Flores, and last September they turned up something none of them had expected: Homo floresiensis. Homo floresiensis was not an ape--it had the signature traits of a homind, such as a bipedal anatomy and small canine teeth. But it wasn't a pygmy human, either. Pygmy brains are in the normal range of variation for our own species. What's more, the floresiensis brain wasn't just small but had a drastically different shape than ours--a shape more like the brain of Homo erectus. This and other anatomical details have led the researchers to conclude that Homo floresiensis branched off from Homo erectus and evolved into a dwarf form.

Here is case-closed proof that today's solitary existence of Homo sapiens is a fluke in the history of hominids. Even 18,000 years ago, at least one other species walked the Earth with us. Exactly how Homo floresiensis went extinct no one knows, but close to the top of the list would have to be ourselves. Neanderthals survived only a few thousand years after humans turned up in Europe, and Homo erectus seems to have disappeared from Indonesia around 40,000 years ago, just around the time humans came on the scene. Perhaps Homo floresiensis lasted longer on Flores because it was harder for humans to reach.

A dwarf hominid on an island is fascinating for another reason--islands are famous for fostering the evolution of dwarf animals, from deer to mammoths. It's possible that the small territory of islands and the lack of competition and predators favors the small. For the first time, hominids have fallen under the same rule. Islands mammals have also been shown to sometimes evolve much smaller brains, and, incredibly, the hominid brain is subject to the same rule. Homo floresiensis's brain shrank down to the smallest size ever found in a hominid. Did Homo floresiensis lose the mental capacity to use tools along the way? The researchers found stone tools in the same site where they found Homo floresiensis, but it's not clear whether Homo floresiensis made the tools, or humans used them (perhaps to kill Homo floresiensis?).

One of the most interesting questions that comes to mind with the discovery of Homo floresiensis is how far back it goes in the fossil record. Just how long did it take for a lineage of hominids to lose half their height and two-thirds of their brain? It may have taken a million years, or a few hundred thousand, or maybe less. In a commentary in Nature, Marta Lahr and Robert Foley of Cambridge point out that it only took 12-foot high elephants on Malta only 5,000 years to shrink to the size of a dog. I've always been a bit skeptical when people forecast dramatic change for our species. But if evolution can produce Homo floresiensis, who knows what a few thousand years on Mars or another solar system could take our descendants?

Update, 11/1/04: Here's a bundle of papers, interviews, and such on H. floresiensis from Nature. Much of it is free.

Last month I blogged about my Scientific American review of Dean Hamer's new book, The God Gene. I was not impressed. It's not that I was dismissing the possibility that there might be genetic influences on religious behavior. I just think that the time for writing pop-sci books about the discovery of a "God gene" is after scientists publish their results in a peer-reviewed journal, after the results are independently replicated, and after any hypotheses about the adaptive value of the gene (or genes) have been tested.

Apparently Time doesn't agree. In fact, juding from this week's issue, they think it's the stuff of cover stories. I should point out that the article itself contains some pretty good interviews with people other than Hamer about their own work--studies of spirituality in twins and the like. But Hamer's work gets the lion's share of space, without any mention that his results haven't been published in a journal (let alone that the last results that got Hamer this sort of press--about a "gay gene"--could not be replicated). Time even copied Hamer's title on their cover, despite the fact that in his book, Hamer backpedals furiously from it, saying that the gene he has identified must be one of many genes associated with spirituality. In fact, the Time article has to backpedal, too. It quotes John Burn, medical director of the Institute of Human Genetics at the University of Newcastle in England as saying:

“If someone comes to you and says, ‘We’ve found the gene for X, you can stop them before they get to the end of the sentence.”

You may be able to stop them from getting to the end of the sentence, but you can't stop the presses.

Update, 11/1: The Time story is no longer available for free. I've linked instead to a Time press release.

I have an article in tomorrow's New York Times about the mystery of autumn leaves. Insect warning? Sunscreen? The debate rages. The one thing I was sad to see get cut for space was the statement by one of the scientists that the answer might be "all of the above." This sort of multitasking is the cool--and sometimes maddening--thing about living things. Very important, and very hard to sort out.

Last week I blogged about the strange story of our past encoded in the DNA of lice. We carry two lineages of lice, one of which our Homo sapiens ancestors may have picked up in Asia from another hominid, Homo erectus. I always get a kick imagining human beings, having migrated out of Africa around 50,000 years ago, coming face to face with other species of upright, tool-making, big-brained apes. It's pretty clear that it happened in Europe, which was occupied by both humans and Neanderthals for several thousand years. But encountering Homo erectus would be even weirder. Studies on DNA suggest humans and Neanderthals share an ancestor dating back half a million years or so. But Homo erectus moved into Asia 1.8 million years ago. These were long-lost cousins, to put it mildly. What's more, they almost certainly had nothing along the lines of human language. Their brains were very different too; they kept making the same stone tools they had been making since they had left Africa. I can't help imagining it would have been an awkward encounter, or even a bloody one. Yet it was close enough for us to pick up their lice.

Hot on the heels of the lice study, a new study on human DNA offers some more support to the idea of a very intimate reunion. Until now, most studies of human genes have pointed to Africa as their origin. If you draw a tree of the various versions of a gene, the deepest branches often belong primarily to living Africans. Some genetic markers are shared almost exclusively by Europeans and Asians, which may have evolved as humans moved out of Africa. These patterns suggested that humans sweeping out of Africa did not interbreed with Neanderthals or Homo erectus. Or, if they did, none of the DNA of those other hominids is around today. But in a paper in press in Molecular Biology and Evolution, University of Arizona scientists report the discovery of a gene that flouts the pattern.

Known as RRM2P4, this gene has its roots in Asia. Over half of people sampled from South China had the oldest version of the gene, while only 1 out of 177 Africans who were surveyed had it. And by studying the variation in different versions of the gene, the researchers concluded that the most recent common ancestor of them existed 2 million years ago. The simplest explanation for this pattern is that at least a few humans and Homo erectus came face to face in Asia and had kids.

The authors point out that the gene they looked at isn't big enough to offer a huge amount of statistical confidence. That will have to wait for other genes with Asian roots, if they're out there. But if RRM2P4 is any guide, humans and Homo erectus didn't just trade lice. Our hominid cousins may not have been able to survive as a species with us in the neighborhood, but all was not war between the species.

Here's the most important thing about The Ancestor's Tale that I couldn't fit in my review. I kept noticing how little Richard Dawkins mentioned the other celebrity evolutionary biologist of our time, Stephen Jay Gould. After all, Gould was a prominent character in many of Dawkins's previous books, cast as the brilliant paleontologist misled by leftist ideology.

Gould was famous for his attacks on adaptationism--the notion that the creative powers of natural selection are behind all sorts of fine points of nature, from jealousy to 11-year cicada cycles. Dawkins was an ultra-Darwinian fundamentalist in Gould's opinion. Gould thought that evolutionary biologists should widen their horizons. They should consider that things that look like adaptations might just be by-products of how organisms develop. They should consider how random catastrophes can override all of natural selection's work, wiping out fit and unfit alike. They should consider how selection may work on many levels--not just with selfish genes, but with populations, and even species. (This was why Gould thought punctuated equilibrium was so important.)

Dawkins would have none of this. He downplayed the importance of developmental constraints, of mass extinctions, and species selection. His attitude towards punctuated equilibrium has been, "Yeah, but so what?"

And then, in The Ancestor's Tale, the battle of Dawkins v Gould disappears. One possibility for the disappearance might be that Dawkins is respecting the dead. (Gould died in 2002.) Perhaps, but the silence is still weird. That's because in this book, Dawkins moves into the heart of Gould territory: the murky realm of evolutionary history. Dawkins has always been at his most eloquent and powerful when he ignores history. His arguments about selfish genes and the like are, at their heart, exquisitely organized reasoning. He did sometimes bring in actual details from biology to these arguments, but only as illustrations of his points. In The Ancestor's Tale, Dawkins takes on 4 billion years of evolution, in all its strange exuberance. The evidence--the fossil record, the relationships of living species revealed by DNA, and so on--dwarfs our explanations for it. We know there were giant scorpions in the oceans, and that they disappeared. But we don't know why. We know that birds survived mass extinctions 65 million years ago, but their close relatives--feathered, flightless dinosaurs--did not. But we don't know why. And so on. You'd imagine that this territory might make an adaptationist a bit anxious.

Dawkins handles himself very well as he moves across this terrain. He knows his natural history, his plate tectonics, and all the rest. He frequently throws up his hands about why the history of life took the turns that it did--although he remains confident that the best way to find the answer is to keep adaptationism first and foremost in mind. Gould shows up only in footnotes. Punctuated equilibrium remains an interesting empirical question but not a major principle. Species selection doesn't even show up in the index.

Yet I thought that sometimes Dawkins didn't acknowledge that some of the episodes in evolution he was writing about still raise some important questions about his selfish-gene centered view. I found this to be the case especially when he wrote about the origin of animals. Animals are multicellular organisms, in which trillions of cells come together as an individual, which then reproduces through just a few sex cells. Animals also descend from a single-celled ancestor. Making that transition isn't simple. A bunch of cells won't just come together and agree that a few of them will get to pass their own DNA on to the next generation. That doesn't make evolutionary sense. The only way to decipher this transition is to view evolution taking place at different levels--at the level of the genes, of the cell, and of the individual. Changes at one level may work against changes at the others, or they may all end up working together. I got interested myself in this subject a couple years ago while writing an essay for Natural History, focusing on the work of Richard Michod of the University of Arizona. It seems to me that the origin of animals is a case where Gould's multi-level selection may work well. Now, Dawkins might disagree, and yet he didn't even mention this challenge to his own views, let alone tear it apart as you'd expect from his previous books. In a 630 page long book, I find this omission puzzling.

It's always possible that Dawkins might eventually accept that in this case multi-level selection is important. He'd probably go on arguing that in most cases a gene-centered approach to life works best. I found it very interesting that he ends the book with a discussion of religion, saying that he suspects that many who call themselves religious would agree with Dawkins (an outspoken atheist) on many of the things he has to say about nature. He describes how "a distinguished elder statesman of my subject" was arguing for a long time with a colleague. The statesman said jokingly, "You know, we really do agree. It's just that you say it wrong."

I imagine Dawkins talking to Gould there.

The New York Times is running my review of Richard Dawkins's new book The Ancestor's Tale this weekend.

I'm particularly grateful at times like these to have a blog, where I can add extra information and the occasional correction.

Towards the start of the review I mention a remarkable tree of 3,000 species. You can download a pdf here. It's files like these that the zoom function were made for.

Towards the end of the review, I say that jellyfish and humans share a common ancestor that lived perhaps a billion years ago. There's plenty of debate about early animal evolution, but a billion years is probably too old--700 million or 800 million would have been better. Maybe I was thinking about fungi instead of jellyfish.

When I have a little more time today, I'll blog about some of the things that I think Dawkins should have included in his book but didn't.

Yesterday I blogged about how the National Park Service is selling a young-Earth creationist book about the Grand Canyon in its stores. Today the Washington Post wrote an article on the subject. It contains a response from the National Park Service, which I find pretty unbelievable. They claim that they are in fact reviewing the matter. The review was supposed to be done in February, but it's been delayed while lawyers at the Interior and Justice Departments "tackle the issue." No deadline is set for the decision, and the book will continue to be sold until one is made.

Tackle the issue? Do these folks really need an extra eight months (and counting) to recognize that the Grand Canyon is millions of years old, and was not formed in Noah's Flood?

The book has been moved from the science section to the inspirational section. But from what I know about it, it's not claiming to offer inspiration but facts. The intellectual cowardice continues.

Continue reading "Further Adventures in Geological Cowardice"

David Appell points to some depressing news about how our government deals with science.

In August 2003, the Grand Canyon National Park Superintendent tried to block the sale of a book in National Park Service stores. The book claims that the Grand Canyon formed in Noah's Flood. No vague ambiguity of the sort you hear from Intelligent Design folks--just hard-core young Earth creationism, claiming that the planet is only a few thousand years old. The folks at National Park Service headquarters stopped the administrator from pulling the book. Geologists cried foul, and NPS promised to review the situation. Meanwhile, the book remained for sale at NPS stores.

And then months passed with nothing. Today a public employees activist group that first publicized this sorry situation announced that it has documents showing that the administration has decided to let the book stay. In fact, there wasn't even any review.

I haven't seen any news pieces yet on this shamefulness, nor have I seen any statement from the National Park Service. From the information we have at hand at the moment, there's only one good conclusion to draw: your government is indifferent to even the most basic facts of science. If it doesn't care about something as well-established as the age of the Earth, you have to wonder what other science it is willing to ignore.

A lot of readers have commented on my recent post about a study that suggests we all share a common ancestor who lived 2,300 years ago. Some people doubted that isolated groups could share such a recent ancestry.

One of the study's authors, Steve Olson (also the author of the book Mapping Human History) sent me the following email yesterday:

"Ensuring a recent common ancestor doesn't take long-range migrations (although contact between the Polynesians and South Americans certainly speeds things up).  All it really requires is that a person from one village occasionally mates with a person from an adjoining village; after that the power of exponential growth, and the dynamics of small worlds networks, take over.  As for counterexamples, I've been looking for five years for examples of populations that were completely isolated, and I've decided that they're rare to the point of nonexistence.  The Tasmanians are a possibility, but it's only 60 miles from Tasmania to Australia -- that no one made that trip in 9,000 years seems counterintuitive to me.  And of course it only takes one person to link two genealogical networks, even though the amount of gene flow represented by that one person may be negligible (though I also think that gene flow in the past has been much more extensive and much more continuous than most people imagine)."

In March, I wrote a post on some tantalizing new findings about the secrets of human evolution lurking in our genome. In brief, researchers at the University of Pennsylvania studied a gene called MYH16 that helps build jaw muscles in primates. In our own lineage, the gene has mutated and is no longer active in jaw muscles. Perhaps not coincidentally, we have much smaller, weaker jaws than other apes. The researchers estimated that the gene shut down around 2.4 million years ago--right around the time when hominid brains began to expand. They suggested that shrinking jaw muscles opened up room in the hominid head for a larger brain.

It's a cool hypothesis, but it may not hold up. Scientists at Arizona State University have followed up on the initial study by anlayzing much larger pieces of MYH16, both in humans and in other species. All told, they studied 25 times more DNA from the gene. In a paper in press at Molecular Biology and Evolution, they report finding a significantly different date for when the gene mutated. Instead of 2.4 million years ago, they get a much older date: 5.3 million years ago.

If that's true, then you can forget any significant link between the evolution of MYH16 and brain evolution. If the Arizona State team is right, the two events are separated by three million years. What's more, the jaws of hominids also remained relatively large after the mutation of MYH16.

The Arizona State researchers do point out an intriguing clue that may eventually lead to a solution to this paradox. The mutation that the Penn team originally argued that the MYH16 gene became useless when a section of DNA in the middle of its sequence was accidentally deleted. Often, when this sort of deletion takes place, DNA-copying enzymes come to a screeching halt at the site of the mutation. With the gene only partly copied, it cannot be turned into a protein. But the Arizona State researchers found signs that the gene did not shut down entirely 5.3 million years ago. The DNA "downstream" from the mutation--in other words, beyond the point where the enzymes stopped copying the gene--has picked up mutations in a pattern that shows no sign of natural selection at work. That's what you'd expect from DNA that doesn't make a gene, since any change will have no effect for good or bad on its owner. But the upstream DNA--the part of the gene that could still be copied--told a different story. It showed signs of having undergone selection. So perhaps the mutation that occurred 5.3 million years ago didn't actually kill the gene, but just amputated it. What the surviving portion of MYH16 did (or still does) remains unknown.

I would wager that this new paper will unfortunately not attract much press. When scientists first come up with an attention-grabbing hypothesis, they're more likely to get a paper accepted to a high-profile journal, and more likely still to get written up by science writers like me. But follow-up work often ends up in the shadows.

That's a shame, because science is actually not made up of single studies that suddenly overturn everything that came before. It's more of a dialectic, as different groups of scientists search for new evidence in order to put hypotheses to new tests. Some hypotheses--such as the idea that chimpanzees are our closest living relatives--have become stronger over time. Others fall away. It would help if more people understood this process. Unfortunately, it seems that a lot of people think science is like building an elaborate sculpture out of glass. If someone discovers that a piece of research is wrong, then it seems as if the whole sculpture cracks and falls to the ground. Creationists are particularly fond of this tactic. They seize on research about evolution that goes against earlier research, and claim that the entire theory of evolution is a fraud. They conveniently ignore all points on which scientists agree. So, for example, the researchers who have published the new findings on MYH16 do not conclude that humans were intelligently designed, MYH16 and all. Instead, they argue that the gene mutated earlier than once believed, and that the full history of this gene remains to be revealed. Science is more like a sculpture made of clay than glass, continually being molded and reshaped to better reflect reality.

Correction, 10/16/04: Changed "ancestors" to "relatives."

Contempt is never wise in biology. The creature that you look down on as lowly, degenerate, or disgusting may actually turn out to be sophisticated, successful, and--in some cases--waiting to tell you a lot about yourself. That's certainly the case for lice.

The human body louse, Pediculus humanus, has two ways of making a living--either dwelling on the scalp, feeding on blood, or snuggling into our clothes and come out once or twice a day to graze on our bodies. For lice, we humans are the world. They cannot live for more than a few hours away from our bodies.Only by crawling from one host to the next does their species escape extinction.

A group of louse specialists recently decided to find out where human lice came from. Have they been riding on our bodies since before we were human? A comparison of the lice that live on different primates shows that they certainly can be very loyal. If you draw an evolutionary tree of primates, and then draw a tree of their lice, they are almost identical. On the other hand, some lice can live on more than one species. And a side-by-side comparison of trees reveals that in some cases they don't form a perfect mirror. In other words, sometimes lice can make an evolutionary leap.

As the researchers report today in Public Library of Biology, they compared human lice to the lice of primates, looking at both their DNA and their anatomy. As earlier research had shown, they found a major split among lice species that live on apes and on monkeys and other primates. That reflects an ancient split in the primates themselves: our ape ancestors diverged from other primates 20-25 million years ago. The variation in louse DNA turns out to act like a sort of molecular clock, showing when they split into different lineages. The molecular clock puts the split between lice that live on humans and chimps at 5.6 million years ago--exquisitely close to the age that's been estimated for humans from studies on both DNA and fossils.

The research suggested that we've carried our lice for millions of years, since before the time of our common ancestor with chimpanzees. But after we parted company with the chimps, the lice have a remarkable story to tell. Human lice split into two lineages. One lineages is found around the world. The second is found only in North America. The worldwide branch all share a common ancestor that lived 540,000 years ago. The North American branch shares a common ancestor that lived 150,000 years ago. And finally, the two branches share a far older common ancestor, which lived a 1,180,000 years ago.

So how did these two strains of the same species become separated and then wind up back on our bodies? The researchers argue that human evolution holds the key. Paleoanthropologists and geneticists still debate over the origins of modern humans, but the rough outlines are becoming clear. The first hominids to emerge that were tall, big-brained bipeds--that weren't just upright apes, in other words--lived about 2 million years ago. They very quickly began to spread out of their birthplace in Africa to other parts of the world. They were in the Caucusus mountains 1.8 million years ago and China 1.66 million years ago. These hominids are generally called Homo erectus, although they may well have consisted of several species, rather than one. And the ranks of Asian Homo erectus may have been boosted by fresh migrations of African hominids when ecological conditions favored another journey out of Africa. But it does appear that Asian populations became pretty isolated from African hominids. The fossils of Homo erectus from a few hundred thousand years ago look pretty distinct from both African hominids and Neanderthals, with very thick skull walls and other peculiar anatomical details. Thirty years ago, most paleoanthropologists would have told you that these Asian hominids probably were the ancestors of living Asians. But that's not what the evidence gathered since then suggests. Instead, it now looks pretty clear that Homo erectus was a very distinct species than Homo sapiens, and became extinct perhaps as recently as 30,000 years ago.

Our own roots can be found in Africa. The oldest clear cut examples of Homo sapiens fossils, found in Ethiopia, date back 160,000 years. By about 100,000 years ago, our species was beginning to diverge into different populations, and these differences can still be found in the DNA of various African groups, such as the Khoisan of Southern Africa (sometimes called bushmen). By 50,000 years ago, humans were moving out of Africa. In Europe, they moved into territory occupied by Neanderthals and their ancestors for some 300,000 years. Neanderthals disappeared by 28,000 years ago. They seem to have been driven into mountainous refuges by the booming population of humans. The story in Asia has always been a bit fuzzier. Humans appear to have gotten to Australia by at least 40,000 years ago, and perhaps much earlier. By 15,000 years ago, some Asian populations of Homo sapiens made their way into the New World through Alaska. Exactly where Homo erectus was on their arrival in Asia, and how long they survived, has never been clear. It hasn't even been clear whether the two species came into contact or not.

You may be able to guess how the louse scientists interpret the data from their parasitic charges. When Homo erectus moved into Asia and became isolated from our own ancestors, their lice became isolated as well. When our own ancestors burst out of Africa around 50,000 years ago, they carried the African lice with them. The most sensational part of the story comes when humans arrive in Asia. The researchers argue that a population of humans encountered Homo erectus and picked up their lice. Their descendants then passed into North America, where they--and their lice--live today. One of the many intriguing implications of this research is that the contact may have occurred in one limited regions--the same region where Native Americans originated in Asia.

This is not the first case where our parasites have preserved our own hidden history. Our tapeworms, for example, can tell us about how our ancestors began eating meat. Malaria reveals how agriculture brought new diseases to humans over the past few thousand years. Helicobacter pylori, the bacteria that trigger stomach ulcers, maps the spread of modern humans. (I go into more detail on some of these examples in my book Parasite Rex.) And the lice probably have more to tell us.

For example, the scientists can't say for sure how humans most likely picked up Homo erectus's lice. The contact definitely had to be intimate. But did it occur when humans drove Homo erectus away from their kills? Or did these two species make love, rather than war? Although the genetic evidence indicates that Homo erectus could not have contributed a significant number of genes to our species, it's possible that they contributed a few. The answer to this question may help show how Homo erectus became extinct, leaving us as the sole hominids left on Earth.

One way to test that possibility will be to look at the other species of lice that live on humans--crabs, or Pthirus pubis. If our ancestors got body lice from Homo erectus during sex, they probably got crabs as well. Somehow, though, I'm guessing that putting together a global collection of crabs may take a little bit longer than the body lice. But it will definitely be worth the wait.

UPDATE: 10/4 9:50 PM: A question occurs to me: why didn't we pick up Neanderthal lice?

UPDATE: 10/5 6:20 PM: The link to the paper is fixed (and the paper is free--bless PLOS!)

Congratulations to Linda Buck and Richard Axel for winning the Nobel Prize for Medicine today. They won for their pioneering work on the 600 or so receptors that we use to smell. As is so often the case these days, the research that wins people the Nobel for Medicine also reveals a lot about our evolution. This February, for example, Buck published a paper in the Proceedings of the National Academy of Sciences, in which she and her colleagues charted the evolutionary history of human olfactory receptors.

As Buck explains, it appears that many olfactory receptor genes mutated beyond repair in our lineage as we came to rely more on sight than smell. Only about half of the olfactory receptor genes in the human genome actually produce working proteins. (You can find working versions of these genes in other animals). Other researchers, however, have found that some human olfactory genes have undergone strong natural selection, which suggests that it's still a good idea to be able to sniff out a piece of rotten meat. (If you want more details on this line of research, you can read an essay I wrote a couple years ago for Natural History.)

And yet, somehow creationsists and their ilk keep a straight face as they continue to tell us that evolution is a dying myth. In this month's Wired, for example, techno-know-nothing George Gilder declares "Darwinian materialism is an embarrassing cartoon of modern science." When Gilder gets to run the Nobel Prize committee, I guess he can take back Buck's medal.

Every now and then you come across a scientific hypothesis that is so elegant and powerful in its ability to explain that it just feels right. Yet that doesn't automatically make it right. Even when an elegant hypothesis gets support from experiments, it's not time to declare victory. This is especially true in biology, where causes and effects are all gloriously tangled up with one another. It can take a long time to undo the tangle, and hacking away at it, Gordian-style, won't help get to the answer any faster.

I was reminded of this while reading Andrew Brown's review of A Reason For Everything by Marek Kohn in the Guardian. The book sounds fascinating. Kohn recounts how a small group of English biologists shaped the course of modern evolutionary biology--in particular, by pondering how adaptation through natural selection could account for just about everything in nature. One of the foremost of these thinkers was William Hamilton, who died a few years ago. Brown writes that "even the colours of the leaves on autumn trees around the grave of Bill Hamilton have been given a meaning by evolution - they are so vivid in order to warn parasites that the tree is healthy enough to repel them."

I wrote about Hamilton's leaf-signal hypothesis here. It is one of those beautifully elegant hypotheses, and some studies have even supported Hamilton's idea that the brilliant colors of autumn evolved as a way for trees to tell insects to buzz off. But readers should not have finished reading my post by thinking, "Well, that sews that question up."

Here's why. H. Martin Schaefer and David M. Wilkinson have written a review of the Hamilton hypothesis which has just gone into press in Trends in Ecology and Evolution. They offer a lot of evidence suggesting that Hamilton may have been wrong--or at least may not have captured the whole picture. They show how a completely different process may be responsible for fall colors. Trees may produce them as they prepare for winter.

When leaves die, their nitrogen, phosphorus, and other nutrients get shipped back into their tree. It's a crucial, carefully orchestrated stage in a tree's life; it will survive on these reserves through the winter. In order to pump the nutrients back into the branches, the leaves need a lot of energy, which they have to generate with photosynthesis. That's where the pigments may come in. Pigments act as a sunscreen for leaves, shielding them from harmful UV rays that can shut down their photosynthetic machinery . What's more, as the leaves ship their nutrients back to the tree, they may produce harmful free radicals as a byproduct. It just so happens that pigments are veritable magnets for free radicals.

If the authors are right, then the evidence that seems to support Hamilton's hypothesis might not actually support it at all. For example, researchers have found that birch trees that display brighter leaves grow more vigorously the following year. You could argue that these trees did so well because they could create such strong warning signals, which warded off insects. But perhaps those bright leaves are just a sign that these trees were doing a particularly good job of protecting their leaves as they stored nutrients for the winter--nutrients that made them more vigorous the follwing spring.

Fortunately, evolutionary biologists can do more than just come up with beautiful hypotheses. They can test them. Schaefer and Wilkinson lay out a list of experiments that could discriminate between the leaf-signal hypothesis and the winter-storage hypothesis. It's even possible that evolution has produced fall foliage in order to both ward off insects and ship nutrients out of the leaf. As beautiful as any one hypothesis may be, it's the interplay of different ideas and the experiments that put them to the test that's most beautiful of all. It would not bother Hamilton one bit, I suspect, if it turned out that the leaves that fell on his grave had taken on their autumn colors for an entirely different purpose.

Evolution works on different scales. In a single day, HIV's genetic code changes as it adapts to our ever-adapting immune system. Over the course of decades, the virus can make a successful leap from one species to another (from chimpanzees to humans, for example). Over a few thousand years, humans have adapted to agriculture--an adult tolerance to the lactose in milk, for example. Over a couple million years, the brains of our hominid ancestors have nearly doubled. Sometimes scientists distinguish between these scales by calling small-scale change microevolution and large-scale change macroevolution. Creationists have seized on these terms and used them to build one of their central canards: that they accept microevolution but can then reject macroevolution. That's a bit like accepting microeconomics--how households and firms make decisions and interact in markets--but then denying macroeconomics--how entire societies produce goods, how inflation rises and falls, and so on. Evolutionary biologists debate fiercely about how macroevolutionary change emerges from microevolution. But they continue to find abundant evidence that the two are a package deal.

I was reminded of the interwoven scales of evolution last week when, just before leaving on vacation, I read a wonderful new paper about how the beaks of baby birds develop. As I drove off sans laptop, I was sure that it would be heavily blogged and reported while I was away. But when I returned I found almost complete silence. So I thought I would do my sm