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.

Here is an error-filled post about evolution by Deepak Chopra, frequent poster to the lefty blog, Huffington Post. I don’t have time to point out the many ways in which Chopra mangles his description of biology, but PZ Myers has. Clear evidence that scientific illiteracy does not respect political boundaries.

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.

Those interested in my upcoming talks may want to visit my main web site. I’ve started to post information about the talks, as well as bringing the archive of my articles up to date. Nothing more depressing than a stale web site.

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.