Blogs / The Loom

Congratulations to all the Macarthur genius grant winners announced today. Their ranks include two evolutionary biologists.

1. Beth Shapiro, at Penn State, studies ancient DNA to understand extinct critters like mammoths and dodos. I’ve embedded a lecture I saw her give over the summer below. [Update: Sorry, sorry--Penn State, not Penn!]

Another winner is Richard Prum from Yale, who I had fortuitously asked to come talk to my writing class this morning. I had my students interview him for a profile. Voila, instant news hook!

The poor students. They were overwhelmed by the torrent of work Prum described, from the sophisticated optical properties of bird feathers to the origin of birds among the dinosaurs to the deep unity of biology and aesthetics. I’ve embedded the Macarthur’s video of Prum from their 2009 Fellows site, where he talks a bit about his stuff.

Recently I took a trip down to North Carolina to spend some time with Brian Hare, an anthropologist at Duke University who wants to understand how human nature evolved. While Hare spends a lot of time in Africa studying chimpanzees and bonobos, he also studies dogs. The social intelligence of dogs is not just interesting in itself, but also for the clues it offers about how we evolved. It’s possible that wolves became dogs in much the same way our chimp-like ancestors became human.

In the newest issue of Time, I’ve written a feature about canine cognition, and scientists like Hare who are trying to plumb its depths. Check it out.

(And be sure to also check out the photoessay of Hare’s new Center for Canine Cognition at Duke, from which this picture comes.)

Romantic poetry and developmental biology have something in common: Goethe. One of botany’s lesser known pioneers, Goethe actually wrote a visionary essay about plants in 1790, which can be summed up in his motto, “All is leaf.” Scientists who are studying the evolution of flowers today hear the echoes of his words. To find out more, check out my lead story in the Science Times section of the New York Times today.

And for more information, check out these recent reviews–

The Evolution of Petal Identity

Reconstructing the ancestral angiosperm flower and its initial specializations

The meaning of Darwin’s ‘abominable mystery’
Reconstructing the ancestral female gametophyte of angiosperms: Insights from Amborella and other ancient lineages of flowering plants

Charles Darwin was interested not just in how new things evolve, but also in how old things disappear. Often, they don’t disappear completely without a trace. We don’t have a visible tail like our primate ancestors did, but we still have a series of little bones tucked away at the bottom of the spine. While it may not function like a full-blown tail, it still anchors muscles around the pelvis. Blind cavefish may not have eyes of the sort found on their cousins in the outside world, but they still start to develop eyes as larva, before the cells start to die away.

Sometimes, though, the only place to look for vestiges of a lost trait is in a genome.

In the journal PLOS Genetics, Mark Springer of the University of California and his colleagues have published an intriguing study of how teeth–and the genes for teeth–have faded away over the past 50 million years. In particular, they looked at enamel, the tough covering that caps the teeth of humans and other vertebrates.

Enamel has three advantages for this kind of study: one is that it fossilizes well. For a lot of species, enamel is often the only thing left behind. Another advantage of enamel is that scientists also have a good understanding of the genes that build it–genes that are similar across a wide range of species. And the third advantage of enamel is that certain lineages of mammals have lost it. Baleen whales, anteaters, and pangolins have all lost their teeth entirely. (Baleen whales grow tooth buds, like cave fish grow eyes, but the buds die back without ever forming enamel.) Sloths, armadillos, pygmy sperm whales, and aardvarks still have teeth, but have no enamel left. This pattern suggests that enamel has been lost independently in several lineages of mammals.

In each lineage, these mammals have lost enamel as they’ve shifted away from depending on hard teeth. As I wrote about here, baleen whales descend from ancestors with formidable teeth for catching prey. But then their ancestors evolved a new way to eat, growing baleen–frond-like sheets of tissue that can filter out krill and other small animals from sea water. As anteaters came to only eat insects, the teeth of their ancestors became not just pointless but a hindrance. Their mouth became finely adapted for shooting a long tongue forward into ant nests. Big teeth would just get in the way.

So where did the enamel go? The scientists decided to test the possibility that the genes for enamel were still in the genomes of toothless mammals, but they had been shut down. In each species’s genome, scientists find a number of so-called pseudogenes, which can no longer encode a protein because of a crippling mutation. A mutation may, for example, insert a “stop” command, so that cells can no longer read the full sequence of a gene and make a full protein. Other mutations can shift a big chunk of DNA over a couple positions, garbling the code. Imagine shifting all the spaces in a sentence to the left. Y ouwou ldg etsomethi ngli kethis.

Despite these devastating mutations, pseudogenes often manage to retain a strong resemblance to their working counterparts. We, for example, have hundreds of pseudogenes that show a striking resemblance to hundreds of other genes that encode a variety of receptors in our noses. So Springer and his colleagues sequenced an enamel-building gene called ENAM in 49 mammal species, including toothless or enamel-less ones to see what happened to the gene along the way.

Their results were pretty much what they expected, but they’re still pretty amazing. There were no frameshift mutations in ENAM among the mammals with teeth. But 17 out of 20 species without teeth or enamel had at least one. In all 20 enamel-free species, a stop command (known as a stop codon) was present. These genes are shot.

The scientists then probed the evolution of the ENAM genes by taking advantage of the fact that only some letters in a gene encode a protein and others are ignored. Mutations that change the structure of a protein may have serious effects on an animal. They may be good effects or really bad ones–in either case, they may change the overall reproductive success of individuals who carry the mutation. On the other hand, silent mutations may have no effect (or at least just a small one).

It turns out that in mammals with teeth, the ENAM gene has experienced something call purifying selection. In other words, very few protein-changing mutations have endured for millions of years because tinkering with the recipe for enamel is a really bad thing to do if you need hard teeth to survive. In mammals without enamel, on the other hand, the ENAM gene evolved in a different way. It experienced what’s known as neutral evolution: the silent mutations and the protein-changing ones have occurred at about the same rate. It just doesn’t matter to the mammals anymore, because the genes are, as I mentioned before, shot.

These genomic vestiges don’t just provide evidence of how teeth were lost. They also provide some clues to when they were lost. By comparing closely related species that don’t have enamel, the scientists could tally up the mutations that had arisen since their last common ancestor. And since neutral mutations tend to pile up at a fairly steady rate, the scientists were able to estimate how long ago the ENAM gene turned from an essential gene to a useless one. In some cases, the scientists predict, paleontologists will find toothless members of these lineages millions of years older than the oldest known fossils without teeth–such as with pangolins, as this figure illustrates.. It is a remarkable convergence, of traces of history recorded in molecules tucked away in anteater cells, and skulls that have managed to turn to stone. But from them, a single picture emerges.

Quick shake of the head, rub of the eyes, and back to some science.

In today’s New York Times, please check out my article about the quest for fossilized color. Birds without color would be like Van Goghs without the paint, and yet for 150 year paleontologists have had to resign themselves to drab fossils of birds, offering little idea of what the birds actually looked like. That’s now changed. It turns out that the microscopic bags of pigment that give feathers color (not to mention squid ink color too) are incredibly tough. Scientists have found them in fossilized feathers, and they’ve pretty conclusively demonstrated that these things are not feather-feeding bacteria, despite a superficial similarity. What’s more, the scientists can now even use the pattern of the bags (a k a the melanosomes) to figure out some things about the color of a 47-million-year-old ex-parrot extinct bird. It had the kind of iridescence you might see on a grackle or a brown-headed cowbird.

You may guess where this is going…There are now lots of dinosaur fossils that have what just about all scientists agree now are feathers. If they’re preserved well enough, you should be able to put them under a microscope and see melanosomes. And if you can make out their patterns…

Stay tuned.

[Images: Grackle via Wikipedia; fossil pictures courtesy of Jacob Vinther]

Over at the Origins blog at Science, I follow up on my essay on the evolution of eukaryotes with a look at a new paper that suggests we are, ultimately, microbes within microbes within microbes. Check it out.

[Image: Wikipedia]

Two of my stories came out this week–one on the near future, and one on the distant past.

1. Global warming is beginning to drive evolution of plants and animals. And soon it will be shifting to high gear. Read more at Yale Environment 360.

2. You, me, and the mushroom over there are all eukaryotes. So are slime molds and Giardia. We all share a number of features that set us apart from prokaryotes like E. coli. The split between eukaryotes and other living things is arguably the deepest in all life. In this week’s issue of Science, I have an essay that looks at how the basic eukaryote cell, complete with nucleus, mitochondria, and all its other bells and whistles came to be. Check it out (here or here). And you can also listen to me talk about the question on this week’s Science podcast here.

The National Institutes of Health funds research on the biology of morality in the human brain, as well as the evolution of  human morality by comparing humans to other primates. Francis Collins, who has been nominated to head NIH, has repeatedly criticized this sort of research–and has used its failure as evidence for the existence of God. In 2008, for example, he said, “I think human altruism can be seen as one of strongest signposts to the existence of a personal God. I can see no fully satisfactory explanation for it coming from biology.”

I’d be curious to know if Collins thinks NIH shouldn’t have funded this research in the past, and if he would cut it in the future. If I were a reporter who went to DC press conferences rather than one that sits at home in his slippers, that’s the question I’d ask–not as a gotcha question, but as a matter on which I cannot figure out an answer based on what he’s said in the past.

Update: Frans de Waal, who does the NIH-funded research on primates I linked to above (and writes lots of interesting trade books on said topic), posted a response I’m pulling up here into the post itself:

Yes, Collins has in the past taken human altruism as proof that God exists, seeing it as a miraculous trait that evolution couldn’t possibly have produced. I disagree, having argued that the building blocks of morality can be found in other animals. I am closer to Darwin than CS Lewis on this. But in response to your blog I must say that I am not sure that Collins will have the power to prevent specific research (such as neuroscience on morality). Furthermore I doubt that he wouldn’t want to know the answers. He is a scientist, after all, and I bet he is open-minded enough to be curious about the outcome of such research even if it doesn’t fully agree with his previous position. Or, am I just being an optimist here?

Thanks for your thoughts, Frans. Of one thing I am sure: the labyrinth of NIH funding is terra incognita for me.

Update #2: Ken Miller, a biologist well known for his books on the relationship between science and religions, has also left a comment:

The worry that Francis Collins would use his position at the NIH to “proselytize” or would not back researchers whom “the religious right dislikes” isn’t grounded in the reality of the man’s life and career.  I’m no more worried about Collins using NIH to advance his religious views than I was about Harold Varmus using the same position to advance non-religious views.  Varmus was a great Director because he was a first-rate scientist who understood how to administer research, and Collins matches him on both counts.

Yes, Collins has written that he doesn’t think that biological evolution can explain the human moral sense.  I disagree with him on that point, even as a fellow Christian.  But Collins’ whole career has been marked by openness, fair-mindedness, and above all, a driving intellectual curiosity.  The over-reaction of those sounding the warning sirens about him is without foundation in fact.  It’s also emotional to the point of irrationality.  PZ Myers has called him “a clown,” and written that “The man is a flaming idjit.”  This comes from a guy who opposes Collins in the name of scientific reason? 

Sweet! Richard Dawkins paid a visit to the Explore Evolution museum exhibit I helped put together. Here’s the first of a series of videos he filmed while he was there, on the evolution of whales. You can watch the others here.

Chimpanzees get AIDS.

This is an important discovery, but what intrigues me most about it is how the discovery was made. It is a story of two kinds of science, both of which are essential to getting a deeper understanding of life, but which today are staggeringly out of balance.

In the 1960s, Jane Goodall carried out some of the first long-term studies on chimpanzees in the wild. Goodall made important observations, noting that chimpanzees can be surprisingly cooperative but also quite violent, with troops engaging in war-like conflicts.

Goodall’s research was part of a long tradition of going to where the animals are, and tracking them for years on end. Goodall didn’t take giant crates of lab equipment with her to Tanzania; instead, she brought patience and careful observation.

Of course, doing this sort of science poses some serious challenges. Field biologists often end up studying relatively few individual animals, because they’re so hard to find. Small sample sizes always make sweeping generalizations risky. Animals in the wild are also embedded in a marvelously complex environment. They are influenced by a vast number of variables–the weather, the food supply, the latest disease outbreak, the latest kerfuffle between the top male and his younger rivals. The state of an animal at any moment may be influenced by many of these variables, making it even harder to uncover important underlying rules of its natural history. And since this kind of science takes so long, it can seem meager if you only learn about it through the papers that the scientists publish.

The contrast between Goodall’s kind of science and, what goes on in, say, a virology lab is enormous. Instead of just watching viruses, scientists can run experiments to test hypotheses–experiments that are controlled with exquisite precision. Scientists can genetically alter viruses to discover how each bit of its genetic material helps (or doesn’t help) it infect its host. They can carefully select the hosts to infect, comparing two sets of hosts for instance that might differ only in one particular cell receptor. They can trace the virus’s journey through the cell and out again; they can sequence viral genes as easily as you might crack open a fortune cookie. And they can churn out many papers a year on what they discover.

The divide between these different kinds of biology has existed for decades, as I wrote in this essay for PLOS Computational Biology. That divide has led to some unfortunate biases. Natural history is sometimes treated like glorified butterfly-collecting. Meanwhile, lab-based molecular biology is sometimes seen as sterile and pointlessly reductionist. But it would be a mistake for one side to think it could live without the other. Understanding the origin of AIDS is a case in point.

In 2007, an estimated 33 million people worldwide had HIV infections, and an estimated 3.1 million people were dying of AIDS-related causes every year. Yet, as diseases go, HIV is a latecomer. Scientists only became aware of it in the early 1980s, when it was still relatively rare, after which it swiftly became a global epidemic. Scientists have tried to search through medical records and blood samples for earlier cases of HIV infection that might have been overlooked. The earliest sample of HIV comes from a blood sample taken from a patient in Kinshasa, the capital of the Democratic Republic of Congo, in 1959.

The mysterious appearance of HIV led to many speculations about where it came from–including accusations that vaccination campaigns introduced it into people with vaccines contaminated with a monkey virus. But when scientists reconstruct the evolutionary tree of the virus and its relatives, they can reject those claims.

As soon as scientists discovered HIV, it was clear that it belonged to a group known as the lentiviruses. Lentiviruses are small particles with spiky knobs on their surface, and they encode their genes in RNA. They infect mammals, such as cats, horses, and primates, typically invading certain types of white blood cells. Genetic studies revealed that HIV is most closely related to strains of lentivirus that infect monkeys and apes–known as simian immunodeficiency virus, or SIV for short. HIV is not actually a single lineage. It is several different strains with different origins.

There are two main forms of HIV, HIV-1 and HIV-2. HIV-2, which is relatively mild, evolved from SIV that live in a monkey called the sooty mangabey. The story of HIV-1, which  causes the vast majority of AIDS cases, is more complicated, as this diagram shows. (It comes from my upcoming book, The Tangled Bank: An Introduction to Evolution.) This tree reveals that it is actually several strains, all of which jumped from chimpanzees.

Scientists first discovered SIV in chimpanzees by looking at captive animals. But in order to get a sense of the true diversity of the virus, they had to leave the relative comforts of laboratories and head out to the places where chimpanzees live. Wild chimpanzees don’t take very well to a blood draw, so scientists developed methods for extracting virus DNA from the feces chimpanzees leave behind. But in order to find those chimp feces, you have to find the chimps (and the trees in which they spend the night).

These studies showed that two subspecies of chimpanzees carry SIV, but HIV-1 has only evolved from one, P. troglodytes trogloydytes, found in west Africa around Kinshasa (marked Ptt on this tree). Goodall’s central African chimpanzees, Pan troglodytes schweinfurthii, have SIV of their own (Pts).

These studies indicate that SIV evolved into HIV as hunters killed apes and monkeys to sell in a growing “bush-meat” industry. Viruses in the blood of the primates could have entered cuts in the skin of the hunters, where a few of them mutated and evolved adaptations to their new host.

Knowing the structure of the HIV tree allows scientists to pinpoint those adaptations. It turns out, for example, that as all three strains of HIV-1 evolved from chimp virus ancestors, they all acquired the same new amino acid in the same position in the same protein. No strain of SIV in chimpanzees produces that amino acid. This mutation altered a gene encoding the shell of the virus, and experiments suggest that it was crucial to the success of the new HIV strains in humans. It’s possible that the mutation allowed the virus to do a better job of manipulating its new hosts into building new copies of itself.

Of course, AIDS is more than just a virus. Once a person is infected with HIV, it may take years for the virus to wipe out his or her immune system, allowing a menagerie of parasites to move in. When scientists studied captive chimpanzees infected with SIV, they didn’t see anything that looked like AIDS. This was intriguing to say the least. Perhaps the chimpanzees and the viruses had coevolved to a peaceful coexistence. When HIV-1 jumped to humans, its evolution took a nasty turn.

But what about chimpanzees out in the real world? Do they get AIDS? That’s a very short question that has taken a very long time to answer. A team of scientists set up shop at Jane Goodall’s study site in Gombe National Park, and took advantage of her decades of field work to track 94 individual chimpanzees for nine years. They searched chimpanzee feces for SIV, and then kept track of the chimpanzees themselves, observing their health, their offspring, and their lifespan. When the chimpanzees died, the scientists autopsied them to see what effect, if any, SIV had on them.

The results, published today in Nature, are stark. Out of the 94 chimpanzees, 17 had SIV. The SIV-infected chimpanzees had a mortality rate 10 to 16 times higher than the uninfected chimpanzees. Fewer infected female chimpanzees gave birth than uninfected ones, and none of their babies survived to a year. Pathologists found that dead infected chimpanzees looked like they had AIDS, with a lower level of immune cells called CD4+ T cells and damaged lymph tissue.

This discovery raises all sorts of questions. The Gombe chimps get sick, but not as sick as humans do from HIV-1. Why? There’s no evidence that SIV jumped into humans from P. t. schweinfurthii. Instead, it jumped three or more times from P. t. troglodytes. As far as anyone knows, those chimpanzees don’t get AIDS. But, then again, nobody has yet published a study like the one that has just come out on the Gombe chimps. What will that study reveal, if anyone ever carries it out? Is P. t. trogolodytes the source of a recent infection of both humans and the Gombe chimps?

And what’s particularly interesting, to me at least, is the fact that scientists had not noticed chimp AIDS before. Robin Weiss, an HIV researcher at University College London, and Jonathan Heeney of the University of Cambridge, published a commentary in Nature in which they suggest that the artificial conditions in which captive chimpanzees live protect them from AIDS. Out in the real world, where chimpanzees face an onslaught of pathogens, infections may activate the immune system in a way that brings on the virus’s attack and, ultimately, AIDS.

In other words, only the slow-cooked science pioneered by Jane Goodall allowed scientists to discover one of the most fundamental facts about a virus that has become one of the most devastating scourges humanity has faced in modern history. Slow-cooked science may provide more clues in the future–but only if its value is recognized, and only if chimpanzees can survive SIV and all the other threats to their survival these days.

[Goodall image: Jane Goodall's Chimpanzees]

In my book  Microcosm  (which has just come out in paperback), I took great pleasure in all the things that something as tiny as E. coli can do. It can survive in frozen soils and stomach acid. It can can build intricate tails which it can then spin hundreds of times a second in order to swim. It can navigate away from the bad and towards the good. It can protect itself from overheating by making just enough protective proteins it needs, with thermostat-like precision. It can survive starvation by folding its DNA into a crystalline sandwich and powering down for months, even years in some cases. It can build microbial cities out of goo, and even commit suicide to help its fellow E. coli survive.

Yet I may have underestimated the brainless intelligence of E. coli. It may even be able to  predict the future.

E. coli has 4000-odd genes, which it can use in various combinations to meet the many challenges it faces. But it does not use all those genes to make proteins and RNA molecules all at once. That would not only be a spectacular waste of energy. Instead,E. coli turns some genes on and keeps others turned off, a bit like playing the keys of a piano. Proteins can clamp onto stretches of DNA near certain genes, for example, making it impossible for the microbe to read them and make the corresponding proteins. When those proteins fall off, or are pried away, the genes can be switched on. (Likewise, other proteins can clamp onto other stretches of DNA and speed up the reading of genes as well.)

One of the most important chapters in the history of modern biology was the discovery of these switches in E. coli. In later years, scientists discovered this basic on-off strategy at work (with lots of variations, of course) in the DNA of all living things.

The way in which E. coli’s genes switch on and off is well-suited to its particular kind of life. For example, E. coli can make proteins that allow it to feed on lactose, the sugar in milk. But most of the time, it keeps the genes for those proteins shut down. If it should encounter lactose, however, the sugar molecule can pull away the repressing proteins, initiating a series of events that leads to E. coli producing a lot of lactose-digesting proteins.

In a case like this, E. coli is responding to something that’s already present in its environment. So-called “higher” species, like us, can also respond to signals of things to come. In fact, thanks to our brains, we can learn new signals. (Think of Pavlov’s dogs, drooling at the sound of the dinner bell.) That led scientists at Princeton to wonder whether E. coli can see into the future as well. It may not have a brain made up of billions of cells, but it does have a complex network of genes that might be able to use information to make predictions about things to come.

The Princeton scientists started by considering E. coli’s natural history. You get regularly infected with new E. coli carried from your hands to your mouth. (Fortunately, the vast majority of these bacteria are totally harmless. Just remember, don’t eat raw cookie dough!) For the E. coli that’s just arrived in your mouth, the world begins to change. It immediately gets a lot warmer, for one thing. Later, as it moves from your mouth down through your gut, the level of oxygen in its environment will drop to near zero. In order to survive, E. coli has to shut down the network of genes it uses to metabolize sugar with the help of oxygen, and then switch on hundreds of other genes for feeding without oxygen.

A sudden rise in temperature is a reliable signal that oxygen will start to drop over the next few hours. The Princeton scientists wondered if  E. coli might use it as a cue to start to prepare for the change. To find out, they experimented on some  E. coli, keeping careful track of which genes were turned on and off when they tweaked the temperature and oxygen levels. It turns out that when E. coli gets warm, it not only switches on heat-defense genes, but also starts making the switch to low-oxygen genes. This switch is remarkable when you consider that it can happen while  E. coli is bathing in a broth rich in oxygen. Unless the oxygen is going to drop soon, this would be a disastrous decision.

It was possible, though, that  E. coli has to switch to a low-oxygen program whenever it defends itself against high temperatures. To test that possibility, the scientists turned  E. coli’s world upside-down. They periodically raised and lowered both the oxygen levels and the temperature in flasks of  E. coli. But now a rise in temperature was followed 40 minutes later by a rise in oxygen, not a drop.

The scientists allowed the bacteria to grow and reproduce for hundreds of generations in this bizarro world. Mutations arose, and beneficial ones spread through the population thanks to natural selection. The scientists then took a look at the bacteria after they had adapted to the new pattern of temperature and oxygen.

Now a rise in temperature prompted a far weaker response from the genes  E. coli uses to survive at low-oxygen levels. The bacteria with mutations that allowed them to continue using oxygen outcompeted the ones that automatically made the switch when the temperature rose. Their experiment suggests that the programs the bacteria use to survive high temperatures and different levels of oxygen are not inextricably linked. The link must be an adaptation, the scientists argue. At some point in the past, the ancestors of E. coli evolved the microbial wisdom that a rise in temperature foreshadows a drop in oxygen.

The Princeton scientists published the details of their experiment a year ago. Now, in the current issue of Nature, a team of Israeli scientists offer evidence that E. coli predicts the future in another way.

The Israeli scientists noted another reliable clue E. coli gets on its journy from mouth to gut. Thanks to the chemistry of our intestines, the upper part of the digestive tract has lactose on offer, but further down in the gut, another sugar called maltose is available. The Israeli scientists wondered E. coli “know” that if it encountered lactose, maltose would be coming soon.

First, they looked at which genes switched on when they fed E. coli different kinds of sugar. Feeding it maltose caused it to make a lot of proteins for digesting maltose. But feeding it lactose caused it not just to make lactose-digesting proteins, but low levels of proteins for digesting maltose too. The effect did not go in the other direction, though. Feeding E. coli maltose does not cause it to make a lot of lactose-digesting proteins.

The Israeli scientists then ran an experiment to see if there was any advantage to E. coli making the maltose proteins in response to lactose. There is indeed. Bacteria that are first exposed to lactose actually grow faster on maltose than bacteria that feed on maltose alone. Other sugars can’t give E. coli this priming advantage. Nor does the advantage work in reverse. Exposing E. coli to maltose does not speed up its growth on lactose.

Finally, the Israeli scientists ran an evolution experiment of their own. They fed E. coli high levels of lactose without any maltose. Under these conditions, making maltose-digesting proteins in response to lactose is a waste of energy. After 500 generations, the scientists found, the bacteria stopped making maltose proteins in response to lactose (although they could still make them in response to maltose itself).

E. coli does not actually learn to make associations the way Pavlov’s dogs learned. The neurons in the brains of the dogs altered their connections. E. coli evolves new connections between its genes over the course of hundreds of generations, as mutations offer up new arrangements, and natural selection favors the ones that speed up the bacteria’s growth. But these experiments do illuminate some of the interesting ways in which evolution resembles learning.

The commentary that accompanies the new paper has the clever headline, “Microbes exploit groundhog day.” In the movie Groundhog Day, you may recall, Bill Murray wakes up day after day only to find that it’s still February 2. After a while, he starts to look clairvoyant to the people around him, because he can anticipate everything that’s going to happen. In some respects, life is a lot like Groundhog Day. Things repeat themselves in a predictable order. Perhaps body temperature and low oxygen are like Groundhog Day for E. coli. Perhaps lactose and maltose are too.

But, of course, a lot of life is not like Groundhog Day. In many cases we can’t predict the future, and so we can’t know exactly what to do now to be best prepared. The same goes for E. coli. So what does E. coli do?

It pretends that it’s betting on horses.

But to find out how it does that particular trick, you’ll have to read about it in  Microcosm.

(Did I mention that it’s now out in paperback? Did I mention how the Boston Globe called it “quietly revolutionary,” and how other people have said equally nice things about it? Just asking…)

Fireflies are the topic of my story on the cover of the New York Times science section tomorrow. It’s the result of a visit I paid last Friday evening to a meadow in Massachusetts, where I listened to Sara Lewis of Tufts University explain the sultry, complex tale of sex, deception, and death that was playing out in front of me.

I first got to know Lewis’s work last summer, when I decided I wanted to include fireflies in my next book, The Tangled Bank: An Introduction to Evolution. Lewis co-authored a fascinating review of firefly biology last year (free pdf from Lewis’s web site). I particularly liked this chart, which shows how different species have evolved different flash signals.

The male, flying around, releases a certain pattern of flashes–a single one second pulse followed by a five secondin the case of Photinus pyralis, for one example. And if a female P. pyralis, sitting on a blade of grass, likes what she sees, she responds three seconds later. Not one. Not six. Three. If she responds at the right interval, he knows he’s found a female of his own species and zeroes in, sending more flashes. She may also be signalling other males at the same time; which male she chooses may come down to subtle features of the flash pattern–for example, a rapid series of pulses as opposed to a slow one.

You can, as I discovered, speak their language with a penlight. You can even play the male or the female, depending on your mood.

There’s lots of strange business going on out among the fireflies. I didn’t have room in the article to describe some of Lewis’s new areas of research. Because female fireflies mate with several males, they can end up with sperm from several males inside them at once. Studies on other animals have suggested that females can choose which male’s sperm they’ll use to fertilize their eggs. Males can also inject chemicals with their sperm that increase their odds of fertilization. It’s clear that in many species, female preferences and male competition can continue after mating ends.

No one knows how this struggle plays out in fireflies. Adam South, one of Dr. Lewis’s graduate students, is investigating this side of the evolutionary equation. He is mating female fireflies with two males apiece and then collecting the eggs they lay. Using DNA tests, he’s determining the paternity of the eggs. Perhaps the males with more attractive flashes have more offspring.

What scientists like Lewis know about fireflies is remarkable, but it’s dwarfed by what they don’t know. Are fireflies on the decline, for example? Unfortunately, there’s no good long-term data. But that’s now an opportunity for some citizen-science you can get involved in. Lewis and some former students have helped organize Firefly Watch, based at the Boston Museum of Science. You can make your backyard part of biology’s new frontier.