\n"; echo $styleSheet; ?>
Home > The Loom > Monthly Archives
The Loom
August 2004


August 30, 2004

Channel Surfing For The Inner ChimpEmail This EntryPrint This Article

While doing some research on human evolution, I stumbled across the web site for a wonderful meeting that was held in March at San Diego to celebrate the sequencing of the chimpanzee genome. You can watch the lectures here. By comparing the chimp genome to the human genome, scientists are discovering exactly how we evolved into the peculiar species that we are. If you find yourself in an argument with someone who claims that evolution has nothing to do with cutting edge science, plunk them down in front of these talks. Without evolution, genomics is gibberish.

(Note--Oliver Baker informs me that this page won't work in Firefox. IE and Safari are fine.)

August 27, 2004

Takes One to Know OneEmail This EntryPrint This Article

Is Intelligent Design the same thing as creationism? The people who back Intelligent Design have spilled an awful lot of ink saying they're different. Even self-proclaimed creationists have tried to claim a difference. Somehow, both of these camps think that any confusion between the two is evidence of the lazy arrogance of evolutionists. In fact, the evidence points towards Intellgent Design being just a bit of clever repackaging to get creationist nonsense into the classroom. (See this useful article.)

A little clarity has emerged over at the new Sarkar Lab Weblog. They've created a "Creationist Faculty," described as a "list of faculty who have spoken in favor of creationism in its traditional form or as intelligent design." They add, "Please feel free to nominate members to this Hall of Shame."

Today they announced an addition--William Dembski, the loudest Intelligent Design advocate out there. Nominated by? Dembski.

Question asked and answered.

Update, 9/1/04: See also this article by Chris Mooney on the political similarities of the creationist and ID movements.

August 26, 2004

Deadly, Tiny, and Ready For Its Close-up, Mr. DeMilleEmail This EntryPrint This Article

bacteriophage2.gifIf you took a census of life on Earth, you'd probably find that the majority of life forms looked like this. It's a virus known as a bacteriophage, which lives exclusively in bacteria. There are about 10 million phages in every milliliter of coastal sea water. All told, scientists put the total number of bacteriophages at a million trillion trillion (10 to the 30th power). Bacteriophages not only make up the majority of life forms, but they are believed to have existed just about since life itself began. Since then, they have been evolving along with their hosts, and even making much of their hosts' evolution possible by shuttling genes from one host to another. Thanks in large part to bacteriophages, more and more bacteria are acquiring the genes they need to defeat antibiotics. Bacteriophages also kill off a huge portion of ocean bacteria that consume greenhouse gases. If you suddenly rid the world of all bacteriophages, the global climate would lurch out of whack.

It may seem strange that the world's most successful life form looks a bit like the ship-drilling robots that swarmed through The Matrix. But the fact is that the bacteriophage is nanotechnology of the most elegant, most deadly sort. To get a real appreciation of its mechanical cool, check out the movie from which this picture comes. (Big and small Quicktime.) The movie is based on the awesome work of Michael Rossmann of Purdue University and his colleagues. (Their most recent paper appears in the latest issue of Cell, along with even more cool movies.) Rossmann and company have teased apart pieces of a bacteriophage and have gotten a better understanding of how they work together. The phage extends six delicate legs in order to make contact with its host, E. coli.. Each leg docks on one of the bacteria's receptors, giving the phage the signal that it is time to inject its DNA. The legs bend so that its body pulls towards the bacterium. The pulling motion makes the base of the phage begin to spin like the barrel of a lock. A set of shorter legs, previously held flush against the base of the virus, unfold so that they can clamp onto the microbe's membrane. The phage's sheath, shown here in green, shrinks as its spiralling proteins slide over one another. A hidden tube emerges, which in turn pushes out a needle, which rams into the side of the bacterium. The needle injects molecules that can eat away at the tough inner wall of the microbe, and the tube then pushes all the way into the microbe's interior, where it unloads the virus's DNA.

It has taken a while, historically speaking, for scientists to come to appreciate just how sophisticated parasites such as bacteriophages can be, a subject I explored at length in my book Parasite Rex. The best human-designed nanotech pales in comparison to bacteriophages, a fact that hasn't been lost on scientists. Some have been using bacteriophages to build nanowires and other circuitry. Others see them as the best hope for gene therapy, if they can be engineered to infect humans rather than bacteria. In both cases, evolution must play a central role. By allowing the phages to mutate and then selecting the viruses that do the best job at whatever task the scientists choose, the scientists will be able to let evolution design nanotechnology for them. From the depths of deep time, one of the next great advances in technology may come. And perhaps some more work in Hollywood, I hope.

August 25, 2004

Spite in a Petri DishEmail This EntryPrint This Article

Spiteful bacteria. Two words you probably haven't heard together. Then again, you probably haven't heard of altruistic bacteria either, but both sorts of microbes are out there--and in many cases in you.

Bacteria lead marvelously complicated social lives. As a group of University of Edinburgh biologists reported today in Nature, a nasty bug called Pseudomonas aeruginosa, which causes lung infections, dedicates a lot of energy to helping its fellow P. aeruginosa. The microbes need iron, which is hard for them to find in a usable form in our bodies. To overcome the shortage, P. aeruginosa can release special molecules called siderophores that snatch up iron compounds and make them palatable to the microbe. It takes a lot of energy for the bacteria to make siderophores, and they aren't guaranteed a return for the investment. Once a siderophores harvests some iron, any P. aeruginosa that happens to be near it can gulp it down.

At first glance, this generosity shouldn't exist. Microbes that put a lot of energy into helping other microbes should become extinct--or, more exactly, the genes that produce generosity in them should become extinct. Biologists have discovered mutant P. aeruginosa that cheat--they don't produce siderophores but still suck up siderophores made by the do-gooders. It might seem as if the cheaters should wipe the do-gooders off the face of the Earth. The solution to this sort of puzzle--or at least one solution--is helping out family. Closely related microbes share the same genes. If a relative scoops up the iron and can reproduce, that's all the same for your genes.

To test this hypothesis, the Edinburgh team ran an experiment. They filled twelve beakers with bacteria they produced from a single clone. While the bacteria were all closely related, half were cheaters and half were do-gooders. They let the bacteria feed, multiply, and compete with one another. Then they mixed the beakers together, and randomly chose some bacteria to start a new colony in twelve new beakers. More successful bacteria gradually became more common as they started new rounds. In the end, the researhers found--as they predicted--that these close relatives evolved into cooperators. The do-gooders wound up making up nearly 100% of the population.

That didn't happen when the researchers put together two different clones in the same beakers. When the bacteria had less chance of helping relatives, the do-gooders wound up making up less than half of the population.

But the biologists suspected that even families could turn on themselves. Mathematical models suggest that the benefit of helping relatives drops if relatives are crammed together too closely. They never get a free lunch--siderophores produced by other, unrelated bacteria. Instead, all the benefits of consuming iron are offset by the cost of producing the siderophores. In the end, the benefit doesn't justify the cost.

The Edinburgh team came up with a clever way to test this prediction out. They ran the same colony experiment as before, but now they didn't take a random sample from the mixed beakers to start a new colony. Instead, they took a fixed number of bacteria from each beaker. This new procedure meant that there was no longer a benefit to being in a beaker where the bacteria were reproducing faster than the bacteria in other beakers. The only way to survive to the next round of the experiment was to outcompete the other bacteria in your own beaker--even if they were your own relatives. The researchers discovered that when closely related bacteria were forced to compete this way, utopia disappeared. Instead, the ratio of cheaters to do-gooders remained about where it started, around 50:50.

The evolutionary logic of altruism also has a dark side, known as spite, which the Edinburgh have explored in a paper in press at the Journal of Evolutionary Biology. (They've posted a pdf on their web site.) It's theoretically possible that you can help out your relatives (and even yourself) by doing harm to unrelated members of your same species, even if you have to pay a cost to do it. You might even die in the process, but if you could wreak enough havoc with your competitors, this sort of behavior could be favored by evolution. Biologists call this sort of behavior spite.

It turns out that many bacteria are spiteful in precisely this way. They produce antibiotics known as bacteriocins that are poisonous to their own species. These poisons take a lot of energy to make, and the bacteria often die as they release them. But these spiteful bacteria don't kill their own kin. Each strain of bacteria that makes a bacteriocin also makes an antidote to that particular kind of bacteriocin. Obviously, evolution won't favor a lineage of microbes that all blow themselves up. But it may encourage a certain balance of spite--a balance that will depend on the particular conditions in which the bacteria evolve.

Understanding the evolution of spiteful and altruistic bacteria will help scientists come up with new ways to fight diseases. (The altruism of P. aeruginosa can make life hell for people with cystic fibrosis, because the bacteria cooperate to rob a person of the iron in his or her lungs.) But bacteria can serve as a model for other organisms who can be altruistic or spiteful--like us. While some glib sociobiologists may see a link between a spiteful self-destructive microbe and a suicide bomber, the analogy is both disgusting and stupid. Yet the same evolutionary calculus keeps playing out in the behavior of bacteria and people alike.

(Update 6.27.04: Did I say siderophiles? I meant siderophores...)
August 23, 2004

Adam and His EvesEmail This EntryPrint This Article

Marriage, we're told by the president and a lot of other people, can only be between one man and one woman. Anything else would go against thousands of years of tradition and nature itself. If the president's DNA could talk, I think it might disagree.

In the 1980s, geneticists began to study variations in human DNA to learn about the origin of our species. They paid particular attention to the genes carried by mitochondria, fuel-producing factories of the cell. Each mitochondrion carries its own small set of genes, a peculiarity that has its origins over two billion years ago, when our single-celled ancestors engulfed oxygen-breathing bacteria. When a sperm fertilize an egg, it injects its nuclear DNA, but almost never manages to deliver its mitochondria. So the hundreds of mitochondria in the egg become the mitochondria in every cell of the person that egg grows up to be. Your mitochondrial DNA is a perfect copy of your mother's DNA, her mother's DNA, and so on back through history. The only differences emerge when the mitochondrial DNA mutates, which it does at a fairly regular rate. A mother with a mutation in her mitochondria will pass it down to her children, and her daughters will pass it down to their children in turn. Scientists realized that they might be able to use these distinctive mutations to organize living humans into a single grand genealogy, which could shed light on the woman whose mitochondria we all share--a woman who was nicknamed Mitochondrial Eve.

Alan Wilson of the University of California and his colleagues gathered DNA from 147 individuals representing Africa, Asia, Australia, Europe, and New Guinea. They calculated the simplest evolutionary tree that could account for the patterns they saw. If four people shared an unusual mutation, for example, it was likely that they inherited from a common female ancestor, rather than the mutation cropping up independently in four separate branches. Wilson's team drew a tree in which almost all of the branches from all five continents joined to a common ancestor. But seven other individuals formed a second major branch. All seven of these people were of African descent. Just as significantly, the African branches of the tree had acquired twice as many mutations as the branches from Asia and Europe. The simplest interpretation of the data was that humans originated in Africa, and that after some period of time one branch of Africans spread out to the other continents.

Despite the diversity of their subjects, Wilson's team found relatively little variation in their mitochondrial DNA. Although their subjects represented the corners of the globe, they had less variation in their genes than a few thousand chimpanzees that live in a single forest in the Ivory Coast. This low variation suggests that living humans all descend from a common ancestor that lived relatively recently. Wilson's team went so far as to estimate when that common ancestor lived. Since some parts of mitochondrial DNA mutate at a relatively regular pace, they can act like a molecular clock. Wilson and his colleagues concluded that all living humans inherited their mitochondrial DNA from a woman who lived approximately 200,000 years ago.

The first studies by Wilson and others on mitochondrial DNA turned out to be less than bulletproof. They had not gathered enough data to eliminate the possibility that humans might have originated in Asia rather than Africa. Wilson's students continued to collect more DNA samples from a wider range of ethnic groups. Other researchers tried studying other segments of mitochondrial DNA. Today they have sequenced the entire mitochondrial sequence, and the data still points to a recent ancestor in Africa. All mitochondrial DNA, it now appears, came from a single individual who lived 160,000 years ago.

More recently, men offered their own genetic clues. Men pass down a Y chromosome to their sons, which remains almost completely unchanged in the process. Y chromosomes are harder to study than mitochondrial DNA (in part because each cell has only one Y chromosome but thousands of mitochondria). But thanks to some smart lab work, scientists began drawing the Y-chromosome tree. They also found that all Y chromosomes on Earth can be tracked down to a recent ancestor in Africa. But instead of 170,000 years, the age of "mitochondrial Eve," they found that their "Y-chromosome Adam" lived about 60,000 years ago.

This discrepancy may seem bizarre. How can our male and female ancestors have lived thousands of years apart? Different genes have different history. One gene may sweep very quickly through an entire species, while another one takes much longer to spread.

In 2001 I wrote an essay on this odd state of affairs for Natural History. At the time, scientists weren't sure just how real the discrepancy was. After all, both estimates still had healthy margin of errors. If mitochondrial Eve was younger and Y-chromosome Adam was older, they might have missed each other by only a few thousand years. On the other hand, if the gap was real, there were a few possible explanations. In one scenario, a boy 60,000 years ago was born with a new mutation on his Y chromosome. When he grew up, its genes helped him reproduce much more successfully than other Y chromosomes, and his sons inherited his advantage. Thanks to natural selection, his chromosome became more common at a rapid rate, until it was the only chromosome left in our species. (This selective sweep might have been just the last in a long line of sweeps.)

Now comes a fascinating new paper in press at Molecular Biology and Evolution. Scientists at the University of Arizona suspected that some of the confusion over Adam and Eve might be the result of comparing the results of separate studies on the Y chromosome and mitochondrial DNA. One study might look at one set of men from one set of ethnic backgrounds. Another study might look at a different set of women from a different set of backgrounds. Comparing the studies might be like comparing apples and oranges. It would be better, the Arizona team decided, to study Y chromosomes and mitochondrial DNA all taken from the same people. Obviously, those people had to be men. The researchers collected DNA from men belonging to three populations--25 Khosians from Southern Africa, 24 Khalks from Mongolia, and 24 highland Papuan New Guineans. Their ancestors branched off from one another tens of thousands of years ago.

The results they found were surprisingly consistent: the woman who bequeathed each set of men their mitochondrial DNA was twice as old as the man whose Y chromosome they shared. But the ages of Adam and Eve were different depending on which group of men the scientists studied. The Khosian Adam lived 74,000 years ago, and Khosian Eve lived 176,500 years ago. But the Mongolian and New Guinean ancestors were both much younger--Adam averaged 48,000 years old and Eve 93,000 years.

You wouldn't expect these different ages if a single Y chromosome had been favored by natural selection, the Arizona team argues. Instead, they are struck by the fact that Khosians represent one of the oldest lineages of living humans, while Mongolians and New Guineans descend from younger populations of immigrants who left Africa around 50,000 years ago. The older people have an older Adam and Eve, and the younger people have a younger one. The researchers argue that some process has been steadily skewing the age of Adam relative to Eve in every human population.

Now here's where things may get a little sticky for the "one-man-one-woman-is-traditional-and-natural" camp. The explanation the Arizona scientists favor for their results is polygyny--two or more women having children with a single man. To understand why, imagine an island with 1,000 women and 1,000 men, all married in monogamous pairs, just as their parents did, and their grandparents, and so on back to the days of the first settlers on the island. Let's say that if you trace back the Y chromosomes in the men, you'd find a common ancestor 2,000 years ago. Now imagine that the 1,000 women are all bearing children again, but this time only 100 men are the fathers. You'd expect that the ancestor of this smaller group of men lived much more recently than the common ancestor of all 1,000 men.

Scientists have proposed that humans have a history of polygyny before (our sperm, for example, looks like the sperm of polygynous apes and monkeys, for example). But with these new DNA results, the Arizona researchers have made a powerful case that polygyny has been common for tens of thousands of years across the Old World. It's possible that polygyny was an open institution for much of that time, or that secret trysts made it a reality that few would acknowledge. What's much less possible is that monogamy has been the status quo for 50,000 years.

People are perfectly entitled to disagree over what sort of marriage is best for children or society. But if you want to bring nature or tradition into the argument, you'd better be sure you know what nature and tradition have to say on the subject.

August 22, 2004

Blog RevivedEmail This EntryPrint This Article

After a couple months of merciless story deadlines, hard disk crashes, and strange viruses that you only find out about once you have kids, the Loom is creaking back to life. Expect several postings this week. For now, let me direct you to a review I wrote a couple weeks ago for The New York Times Book Review about Devil in the Mountain, a book about the Andes. The author, an Oxford geologist, dissects these mountains like a surgeon cutting open a living person. It reminded me of the times I've driven around with geologists; all of the landscape that blurs past most of us is a vast palimpsest to them, and waving their hand out the window, they tell you about hundreds of millions of years of mountain building and destruction. Short of grabbing a geologist for a ride, I'd suggest getting the book.