If you were this man, you’d be smiling too.

The man is Lee Berger, a paleoanthropologist at the University of Witwatersrand in South Africa. He’s holding the skull of Australopithecus sediba, a 1.98 million year old relative of humans, otherwise known as a hominin. In April 2010 Berger and his colleagues first unveiled the fossil in the journal Science. As I wrote in Slate, Berger argued that A. sediba was the closest known cousin to our genus Homo. Hominins branched off from other apes about 7 million years ago, but aside from becoming bipedal, they were remarkably like other apes for about five million years. Among other things, they were short, had long arms, and had small brains. Berger and his colleagues saw in A. sediba what biologists often find in transitional forms–a mix of ancestral and newer traits. It has Homo-like hands, a projecting nose, and relatively long legs. It was intermediate in heigh between earlier hominins and the tall Homo. And it still had a small brain and long arms. (In August, Josh Fishman wrote a feature for National Geographic on A. sediba, complete with excellent reconstructions.)

It wasn’t just finding such a potentially significant fossil that would make you smile if you were Lee Berger. It’s how much stuff he and his colleagues have found. The skull that Berger holds would be enough to keep several scientists busy for years. But Berger and his team have much more. In fact, A. sediba is, in some ways, now even better represented than far more recent hominin relatives.

Today, Science has turned over much of this week’s issue to follow-up papers from Berger’s team, in which they share some of the goodies. Here, for example, is A. sediba’s hand. Before this specimen came to light, paleoanthropologists had much less to look at to study the origin of the human hand. The best specimen came from a 1.75 million year old hominin called Homo habilis. It got the name Homo in part because the fossils were found along with stone tools, which were considered a sign of a very human-like creature. Researchers also found bones from its hand–but only 13 fragments. In this picture of A. sediba‘s hand, just about every bone is real. This is what paleoanthropologists dream about at night.

Tracy Kivel, a paleoanthropologist at the Max Planck Institute, led a team of researchers who compared A. sediba’s hand to the hands of humans, chimps, gorillas, and extinct hominins. They found even more mingling of old and new traits than before. The hand has ridges for powerful muscles that run up the length of the hand. Chimpanzees have muscles like these, which give them stronger grips as they climb around in trees. Earlier hominins have them too. We don’t. Instead, we have long thumbs and fleshy pads on our finger tips, which are great if you’ve come to depend on your skill to make and use tools. A. sediba has them too.

Scientists have found likely hominin stone tools dating back 2.6 million years ago; last year a team of researchers kicked up some controversy by claiming to have found signs of stone tools 3.4 million years ago. It’s clear that by the time A. sediba came on the scene, hominins had been using stone tools for hundreds of thousands of years. It’s too bad that Berger and his colleagues haven’t found any tools alongside A. sediba’s bones, to see what they could do with these transitional hands. Then again, why should he get all the fun?

Things got particularly intriguing when Kivel and company compared A. sediba‘s hand to Homo habilis’s. Remember, Homo habilis is about 250,000 years younger than A. sediba. Yet A. sediba‘s hand is actually more like our own than that of Homo habilis. It’s got some wrist bones that are shaped to handle strong forces transmitted from the thumb–the sort of forces you might expect from whacking stones together to make a cleaver, for example. Evidence such as this suggests that Homo habilis branched off first from the ancestors of A. sediba and later hominins like ourselves, and then later A. sediba branched off from our own lineage. Along the way, the hand gradually became less adapted for tree-climbing, and acquired more traits we use to handle tools.

In other papers, scientists take a look at A. sediba‘s brain and hips. The two are more intimately associated than you might think at first. We have huge brains even at birth, which make child-bearing a tricky proposition in our species, because they have to be able to pass through the birth canal. We humans have wide hips compared to other apes, and some researchers have argued that they evolved in tandom with our expanding brains. (See this column I wrote recently for more compensations in our bodies for big brains.) But it turns out that A. sediba–which had a small brain–already had broader hips than earlier hominins. Whatever drove its hip expansion, a big head wasn’t it.

While the A. sediba brain was small, it demonstrates that in hominin brain evolution, size isn’t everything. The skull Berger holds here contains a beautifully preserved cavity inside. When he and his colleagues put the fossil in a scanner, they were able to reconstruct the shapes of a lot of the left hemisphere of the brain and the front chunk of its right. The shapes of some parts of the brain (in particular, a part of the brain called orbitofrontal cortex) are more like our own than like earlier hominins.

Reading this, I can’t help but dabble in a little paleo-phrenology. The orbitofrontal cortex is a crucial node in our emotional network, where neurons assign value to things and can tamp down or ramp up our automatic responses of fear and delight. Did a glimpse of human feelings mark this great transition, long before human-sized brains evolved?

I doubt scientists will ever answer that question, but not to worry: there are many more answers A. sediba will be able to provide.

[Images: Berger, courtesy of Lee Berger and University of Witwatersrand; hand and pelvis by Peter Schmid, courtesy of Lee Berger and University of Witwatersand; brain, photo by ESRF/KJ Carlson, courtesy of Lee Berger and the University of Witwatersrand]

In tomorrow’s New York Times, I take a look at a new study on the generosity of chimpanzees. Check it out. (And also check out Ed Yong’s take at Not Exactly Rocket Science.)

[Image courtesy of Frans de Waal]

To understand how we evolved, we have to understand where we evolved. Natural selection exists because the environment is kinder to some individuals than others. Depending on the species, that environment may be a lake miles underneath Antarctic ice, an alpine meadow near the top of a mountain, or an oxygen-free swamp in the sweltering tropics. Each habitat creates its own set of conditions in which individuals thrive or die. We humans are no different. We are the product of where we have lived.

A century ago, paleontologists thought humans evolved in Central Asia. At the time the only known fossils of an ancient human relative (what we now call a hominin) came from Indonesia. The idea of humans evolving in dank rain forests did not appeal to Western scientists who lived in temperate climes. They looked to Central Asia’s windswept plains. In 1926, the American paleontologist Henry Fairfield Osborn laid out this line of thinking in an essay called “Why Central Asia?”

“In that environment, the struggle for existence was severe and evoked all the inventive and resourceful faculties of man,” he wrote. “While the anthropoid apes were luxuriating in the forested lowlands of Asia and Europe, the Dawn Men were evolving in the invigorating atmosphere of the relatively dry uplands.”

It’s hard to imagine worse timing for such a declaration. In 1925, the year before, Raymond Dart discovered the skull of a another hominin in South Africa. It was much older than the one in Indonesia, and it was a lot more ape-like. And since then, paleoanthropologists have found many more fossils of very old hominins in Africa, from South Africa to Kenya and up to Ethiopia and Chad. Hominins first split off from the ancestors of chimpanzees and bonobos (both found only in Africa) about seven million years ago. The oldest hominin fossils date back to about that age, and from seven million to 1.8 million years ago, the fossil record was exclusively African. Only then did hominins start popping up in places like Indonesia and the Caucasus Mountains. Hominins also continued to inhabit Africa, and evolve into new species. The first fossils of Homo sapiens, dating back about 200,000 years ago, are from Ethiopia.

While Osborn was wrong about the place where humans evolved, his vision of the invigorating atmosphere of dry uplands survived. Dart himself wrote in Nature that South Africa offered the same challenging grasslands as Central Asia.

“We must therefore conclude that it was only the enhanced cerebral powers possessed by this group [us] which made their existence possible in this untoward environment,” Dart concluded. For humans to split off from apes, he wrote, they required “a more open veldt country where competition was keener between swiftness and stealth, and where adroitness of thinking and movement played a preponderating role in the preservation of the species.”

Dart offered an early version of what came to be known as the “savanna hypothesis”–that moving from the forests to open grasslands drove the evolution of the hominin lineage, including the evolution of walking upright, a big brain, and even the loss of body hair.

In the decades that followed, scientists tried to reconstruct the ecosystems in which hominins lived. Plant fossils were scarce, but in many cases–particularly in the Rift Valley of East Africa–these studies pointed to open, savanna-like environments.

By the 1990s, however, things started to get confusing. James Shreeve, writing in this 1996 Discover article , explained how paleoanthropologists were finding evidence that the early hominins might actually have lived in more closed woodlands. The debate rolled on, fueled in part by the scarce information scientists had to rely on.

Eighty-six years after Dart first presented the savanna hypothesis in Nature, the journal has now published a spectacular chronicle of the environment in which our ancestors evolved. Thure Cerling of the University of Utah and his colleagues found a way to overcome the scarcity of plant fossils. Plants absorb carbon from the atmosphere to build their wood, stems, and leaves. Carbon in the atmosphere may have different numbers of neutrons–it may be isotopically “heavy” or “light.” Different kinds of plants will end up with a different balance of light and heavy carbon in their tissues. When the plants die, they add their carbon isotopes to the soil. And the soil itself can sometimes turn to rock–a substance known as a paleosol.

Cerling and his colleagues went to African forests and grasslands and measured the carbon isotopes in the soils. They found they could accurately predict the percentage of woody plant cover from the isotopes alone. With this method in hand, they then analyzed 1300 samples of paleosols that formed over the past seven million years from two sites that have yielded some of the richest troves of hominins: the Awash Valley in Ethiopia, and the Omo-Turkana Basin in Kenya. The result is a “tour de force,” according to Harvard paleoanthropologist Daniel Lieberman (who was not involved in the study).

Here is a massive graph summarizing their findings, which will become the benchmark against which future studies of hominin evolution will be measured.

The further to the left the curves are, the more wooded the habitats. The further to the right, the more open they were. In between are bars showing the age of different hominin fossils. The further to the right the bars are, the more small-brained and big toothed they are. The more to the left, the more like us they are. (You can see a bigger version of the graph here.)

Once you’ve grokked this image, join me at the bottom for an explanation of what it all may mean.

Cerling and his colleagues have found that seven million years ago, grasslands with sparse trees existed at these sites. The woody cover increased over the next few million years, reaching its greatest extent about 3.6 million years ago, when the sites were 40-60% woody cover. Then the woods began to retreat. By 1.9 million years ago, there was no place left with more than half woody cover. The environments continued to open up, the trend continuing till today.

I asked Lieberman, who studies the evolution of human anatomy, how he thinks hominin evolution played out against this ecological backdrop.

“Chances are we split from other apes in the forest,” Lieberman told me. He notes that chimpanzees, bonobos, and gorillas all live in the forest today. The fact that we don’t find early forest hominins is probably due to the fact that closed forests are lousy places for fossils to form. It’s probably no coincidence that scientists have found practically hardly any fossils of chimps or gorillas. They’ve lived in the wrong place.

Another crucial fact to consider is that the earliest known hominins have a number of features that hint that they were no longer knuckle walkers. A number of researchers argue that while they couldn’t walk as fast as we can and probably couldn’t run at all, they were already bipedal. So even though the earliest hominin fossils come from lightly wooded East African grasslands, Lieberman suspects that the origin of bipedalism took place earlier, and it took place in forests elsewhere on the continent. (Another paleoanthropologist, John Fleagle, expressed a similar sentiment to me.)

Lieberman suggests that the earliest hominins adapted to the margins of those early forests, where they had to travel further from tree to tree to find fruit. He and his colleagues have found that it’s four times more efficient for a human to walk a given distance than it is for an ape to knucklewalk. Saving energy on these trips could have translated into more babies.

By about seven million years ago, studies like Cerling’s now suggests, hominins were already moving around on two legs through open woodlands. Hominins evolved to be more efficient walkers. They also acquired big teeth and jaws. Lieberman argues that hominins need this new mouth equipment so that they didn’t have to rely on fruit alone. They could also chew on harder, tougher plants like tubers, which served as fall-back foods in the open woodlands.

Although tree cover increased for a couple million years, forests never came to dominate the East African landscape in the past seven million years. And when open grasslands returned with a vengeance, hominins underwent a dramatic change. They got tall and acquired traits that Lieberman argues were adaptations for running. Their teeth and jaws got small; their snouts disappeared.

Lieberman argues that this change marks a new way in which hominins coped with the increasing grasslands: they became hunter-gatherers, traveling long distances to stalk game. And once they began to enjoy this high-protein diet, one more change occurred: the energy-hungry hominin brain was able to expand towards its current size.

But he is quick to point out that there are some important facts about hominin evolution that don’t fit neatly into the scenario he sketched out for me, and a lot of other crucial facts thtat remain to be discovered. “Anybody who isn’t confused doesn’t know what’s going on,” he said. At least scientists now have a better backdrop for finding out exactly what did happen on the way to Homo sapiens.

[Image: Samburu National Reserve in Kenya, Thure Cerling, University of Utah]

Our cells are packed with various protein-stuffed sacs, each dedicated to carrying out essential tasks. One kind of organelle is peculiar, though. Mitochondria are jellybean-shaped structures whose jobs include making the fuel that our cells use to power everything they do. What makes mitochondria strange is that they carry their own DNA. It’s not a lot of DNA–just 37 genes–but mitochondria can make extra copies of it as they grow and divide. In other words, they act an awful lot like bacteria.

About a century ago, Russian biologists proposed that mitochondria actually started out as bacteria, which set up house in our single-celled ancestors. In the 1960s, University of Massachusetts biologist Lynn Margulis resurrected the idea, pointing to certain features in mitochondria, like their double membrane, found in bacteria but not in other organelles. In the 1970s, biologists began to invent the tools that allowed them to look at the DNA in mitochondria. As predicted, that DNA matched DNA from bacteria, not from animals.

Acquiring mitochondria over 2 billion years ago was a pivotal moment in our evolution. We are eukaryotes, as are trees, mushrooms, and amoebae. We all carry mitochondria (or organelles that started out as mitochondria). Once our eukaryotes acquired mitochondria, they could produce so much fuel that they could get very big. Eukaryote cells are much bigger than bacteria, and eukaryote cells have, on several occasions, stuck together to form multicellular bodies. You can thank your mitochondria for being more than a germ.

But what kind of bacteria did mitochondria come from? This is a lot harder to answer, because we know so little about the diversity of bacteria in the world. When scientists trace the origins of an organism, they compare it to other living things. In the case of birds, for example, scientists have compared them to other land vertebrates. In the big scheme of things, land vertebrates have never been particularly diverse. Scientists have a pretty good grasp of every group of land vertebrates that ever lived, and so they’ve been able to carefully compare birds to all of them. Birds did not evolve from frogs. They did not evolve from skunks. They evolved from feathered dinosaurs. There’s still plenty to learn about exactly which fossil dinosaur was the closest relative to the first birds. But in general terms, the origin of birds is pretty much settled.

When it comes time to compare mitochondria to bacteria, however, scientists face a much tougher challenge. Consider this: there are 5,000 species of mammals alive today. It’s big news when a mammalogist stumbles across a single new species of mammal. If you dig up a spoonful of dirt from your front yard, there may be 10,000 species of bacteria in it–many of which are new to science. If you’re anything like me, even your bellybutton is rife with exotic, undescribed bacteria.

This diversity makes comparisons difficult. It’s as if alien scientists wanted to figure out where humans came from, but they could only compare us to tulips and E. coli. Our DNA shows we are closer to tulips than E. coli, and so the alien scientists might be tempted to declare that we started out as flowers. If the alien scientists could compare the millions of eukaryote species that human scientists know about, however, they could see that plants and animals became multicellular on their own. We have no petals in our past.

Over the past twenty years, scientists have been finding bacteria that are closer and closer to mitochondria, and, in the process, they’ve been zeroing in on what the ancestors of mitochondria might have been like. Recently, J. Cameron Thrash at Oregon State University and his colleagues published a big new study of mitochondria and their relatives that brings them into even sharper focus. The open-access paper appears in the new journal Scientific Reports.

Initially, scientists recognized that mitochondria belonged to a big group of species called alphaproteobacteria. Then researchers sequenced a genome of Rickettsia, a group of alphaproteobacteria that cause diseases like typhus. They found a striking match between Rickettsia and mitochondria. Particularly intriguing was the fact that Rickettsia can only replicate inside eukaryote cells. One could imagine mitochondria starting out the same way, infecting some amoeba-like ancestor. Yet some researchers disputed this conclusion, arguing that the data wasn’t strong enough.

Then scientists went trawling for new bacteria in the oceans and, as they always do, found some surprises. They found new kinds of Rickettsia bobbing in the sea. This lineage of Rickettsia, called SAR11, does not need to infect a host to survive. Instead, this tiny microbe breathes oxygen and slurps up dissolved carbon.  Scientists now recognize SAR11 as one of the most successful lineages in all life: they make up 25% of all the bacteria in the ocean.

Thrash and his colleague did a massive comparison of SAR11 and other  bacteria, analyzing over 60 entire genomes. They concluded that SAR11 are more closely related to mitochondria than other bacteria, including other Rickettsia.

It’s possible, they argue, that our mitochondria did not start out as typhus-like pathogens. Instead, we might look to SAR11 for some clues. SAR11 bacteria breathe oxygen–a capacity that mitochondria gave to our ancestors. SAR11 bacteria also have extremely small genomes–probably because the bacteria were living on a meager food supply and so natural selection favored individual microbes with few genes. It’s likely that once mitochondria became established in our cells they lost many genes that they no longer needed. But this new research hints that they were already tiny, lean bacteria when they took their first step inward.

I can remember first learning of the history of mitochondria, and marveling that we are the offspring of a collective, of a cell that became a home for bacteria, which gave it a new breath of life. Now I will marvel again when I look out at the ocean and realize how, until recently, we didn’t know that our bacterial residents are cousins to an inconceivable number of microbes in the sea.

[Image: Wellcome Images]

[Update--Changed Giardia to E. coli. Dang polytomies]

In tomorrow’s New York Times, I’ve got a story about evolutionary biologists who make New York their Galapagos Islands. Working on this story was great fun–I traipsed around Manhattan parks and medians, checking out mice and ants and salamanders. I spoke to other researchers who study plants, fish, and bacteria in and around the city. All of them observe evolution unfolding in what might seem like a very unnatural place. But after four billion years, nothing can stop evolution. Not even New York.

The Times has posted some of Damon Winter’s wonderful photographs for the story along with some audio from some of the scientists I describe. You can also listen to the new podcast, which features the story too (link to come).

[ Photo: Creative Commons: NatalieTracy on Flickr ]

For several decades now, biologists have been puzzling over sex. In some ways, it seems like a huge waste of effort.

Sexual reproduction requires splitting a species into two sexes, only one of which will be able to produce offspring. There are some species of animals that do without males; the females simply trigger their eggs to develop into embryos without any need for sperm. All the offspring of an asexual animal can produce offspring of their own, instead of just half. So it would make sense that genes that gave rise to asexual reproduction would win out in the evolutionary race.

Clearly that hasn’t happened. The world is rife with sex. Animals do it. Plants do it. Even mushrooms do it. So evolutionary biologists have carried out a number of studies to get an answer to the question, “Why sex?”

In 2009, I wrote an essay for Science about this research. If I had been writing that essay today, I’d have focused some attention on an elegant experiment on the sex life of a humble worm. It gives a big boost to the long-floated idea that evolution favors sex because it lets hosts fight better against parasites.

Allow me to explain by self-plagiarizing:

In the 1970s, several researchers built mathematical models of how parasites influenced the evolution of their hosts and vice versa. Their research suggested that both partners go through cycles of boom and bust. Natural selection favors parasites that can infect the most common strain of host. But as they kill off those hosts, another host strain rises to dominate the population. Then a new parasite strain better adapted to the new host strain begins to thrive, leaving the old parasite strain in the dust.

This model of host-parasite coevolution came to be known as the Red Queen hypothesis, after the Red Queen in Lewis Carroll’s book Through the Looking Glass, who takes Alice on a run that never seems to go anywhere. “Now here, you see, it takes all the running you can do to keep in the same place,” the Red Queen explains.

The Red Queen conundrum, some researchers have argued, may give an evolutionary edge to sex. Asexual strains can never beat out sexual strains, because whenever they get too successful, parasites build up and devastate the strain. Sexual organisms, meanwhile, can avoid these dramatic booms and busts because they can shuffle their genes into new combinations that are harder for parasites to adapt to.

Red Queen models for sexual reproduction are very elegant and compelling. But testing them in nature is fiendishly hard, because biologists need asexual and sexual organisms that share the same environment and parasites.

Scientists have found some mixed populations in the wild where they’ve made some important discoveries. But it’s also possible to test the Red Queen in laboratories. It’s not easy, because scientists need to bring together a host that can reproduce sexually and asexually with a parasite, and then they both have to be able to evolve in response to each other. But that’s what a team of scientists at Indiana University managed to do recently.

As they describe in a paper published today in Science, they reared populations of a tiny worm called Caenorhabditis elegans. C. elegans are born either as males or hermaphrodites. A hermaphrodite worm can fertilize its eggs with its own sperm, or it can seek out a male. The worms typically don’t have a lot of sex, and the rate at which they do is partly programmed into their genes. The Indiana team of scientists were able to engineer the worms so that they could have no sex at all, or could only reproduce through sex.

For their parasite, they chose a species of soil bacteria called Serratia marcescens. Soil bacteria are the regular prey of C. elegans, but if they slurp up S. marcescens by accident, they get sick and can die in under 24 hours. Previous studies had shown that the worm can evolve stronger resistance to the germ, and the germ can evolve to be deadlier for the worm. So the Indiana researchers set about combining their evolution into one big experiment.

They mixed together worms and germs in several different arrangements and let them duke it out for 30 worm generations. In each trial, the worms were either sexual or asexual.  In some trials, the bacteria coexisted with the worms for the whole experiment, so that they could evolve along with the worms. In other trials, the worms were repeatedly presented with the same, fixed strain of S. marcescens. In other words, the bacteria could not evolve. And in control experiments, the worms enjoyed a Serratia-free life.

As this graph to the left shows, the asexual worms that faced co-evolving germs were annihilated in just 20 generations. (“Obligate selfing” means no sex.) If the germs couldn’t evolve, however, the asexual worms did fine. The scientists also tested the bacteria for deadliness after the experiments were over. They found that the bacteria that were allowed to co-evolve with the asexual became much deadlier. The co-evolving sexual worms, on the other hand, suffered far lower mortality rates from their germs.

In another experiment, the scientists started out with ordinary worms, which only had sex about 20 percent of the time they reproduced. Again, they exposed the worms to unchanging bacteria, or co-evolving ones, or no bacteria at all. The graph to the right says it all. The worms not exposed to the bacteria went on having infrequent sex. The worms that could evolve but faced fixed bacteria had more sex for a while, but eventually crashed back down to their original levels. The coevolving worms, on the other hand, became mostly sexual.

In each of these results, the Red Queen has left her mark. Far from being a waste of time, sex may save organisms from a swift oblivion.

[Images: turtles via Creative Commons from man of mud/Flickr. C. elegans via Creative Commons licence from AJ Cann/Flickr.]

(Update: paper link fixed)

I just got back yesterday from the annual meeting of the Society for the Study of Evolution. It took place in a big hotel on the outskirts of Norman, Oklahoma, during a windy heat wave that felt like the Hair Dryer of the Gods. It had been a few years since I had last been to an SSE meeting, and I was struck by how genomic everything has gotten. No matter how obscure the species scientists are studying, they seem to have outrageous heaps of DNA sequence to analyze. A few years ago, they would have been content with a few scraps. Fortunately, SSE hasn’t turned its back on good old natural history. There were lots of fascinating discoveries on offer, about species that I had assumed had been studied to death. My favorite was a talk about the rough-skinned newt, the most ridiculously poisonous animal in America.

The scientific tale of the rough-skinned newt begins five decades ago, with a story about three dead hunters in Oregon. Reportedly, the bodies of the hunters were discovered around a camp fire. They showed no signs of injury, and nothing had been stolen. The only strange thing about the scene was the coffee pot. Curled up inside was a newt.

In the 1960s, a biologist named Butch Brodie got curious about the story. The newt in the coffee pot–known as the rough-skinned newt–has a dull brown back, but when it is disturbed, it bends its head backward like a contortionist to reveal an orange belly as bright as candy corn. Bright colors are common among poisonous animals. It’s a signal that says, in effect, “If you know what’s good for you, you’ll leave me alone.” Brodie wondered if the newts were toxic, too.

Toxic, it turns out, doesn’t do the newts justice. They are little death machines. The newts produce a chemical in their skin called tetrodotoxin, or TTX for short, that’s made by other poisonous animals like pufferfish. Locking onto sodium channels on the surface of neurons, TTX blocks signals in the nervous system, leading to a quick death. In fact, TTX is 10,000 times deadlier than cyanide. While we may never know for sure what killed those three Oregon hunters, we do know that a single rough-skinned newt could have easily produced enough TTX to kill them, and have plenty of poison left over to kill dozens more.

Now, if the whole idea of evolution makes you uneasy, you might react by saying, “That couldn’t possibly have evolved.” Experience has shown that this is not a wise thing to say. Brodie said something different: the most plausible explanation for a ridiculously poisonous animal is that it is locked in a coevolutionary arms race with a ridiculously well-defended predator. Another biologist mentioned to him that he’d seen garter snakes dining on rough-skinned newts, and so Brodie investigated. He discovered that garter snakes in rough-skinned newt territory have evolved peculiar shape to the receptors on their neurons that TTX would normally grab.

The coevolution of newts and snakes became a family business. Brodie’s son, Edmund, grew up catching newts, and today he’s a biologist at the University of Virginia. Father and son and colleagues have discovered that snakes have independently evolved the same mutations to their receptors in some populations, while evolving other mutations with the same effect in other populations. They’ve also found that both newts and snakes pay a cost for their weaponry. The newts put in a lot of energy into making TTX that could be directed to growing and making baby newts. The evolved receptors in garter snakes don’t just protect them from TTX; they also leave the snakes slower than vulnerable snakes. They’ve studied newts and snakes up and down the west coast of North America and found a huge range of TTX potency and resistance. That’s what you’d expect from a coevolutionary process in which local populations are adapting to each other in different environments, with different costs and benefits to escalating the fight.

This story is so irresistible that I’ve written about it twice: first, ten years ago in Evolution: The Triumph of an Idea,, and then in updated form last year in The Tangled Bank. I figured that the Brodies et al had pretty much discovered all there was to know about these creatures. But in Oklahoma, I discovered that they had missed what is arguably the coolest part of the whole story.

Think about it: you’re a female newt, you’ve fended off attackers with a staggering amounts of poison in your skin, and now you want to pass on your genes to your descendants. You lay a heap of eggs in a pond, and what happens? A bunch of pond creatures come rushing in and have a feast of amphibian caviar.

What could you possibly do to ensure at least some of your offspring survived? Well, you have an awful lot of TTX in your system. You have enough of the stuff to give your eggs a parting gift to help them out there in the cruel, predator-infested world. Make your eggs poisonous.

That is exactly what female newts do. In fact, they load their eggs with TTX. To figure out if this poison provided a defense against predators, the Brodies and their students traveled to a group of ponds in central Oregon that are home to thousands of rough-skinned newts apiece. They collected dragonflies and other aquatic predators from the ponds and put them in buckets filled with newt eggs, along with muck from the pond bottoms. The scientists found that almost none of the predators would touch the newt eggs. Since these predators eat plenty of eggs of other species, this result shows that TTX does indeed help the newt eggs survive.

But there was one exception. Caddisfly larvae turned out to relish the newt eggs. In fact, the caddisflies actually grew bigger if they were supplied with newt eggs and pond muck than with pond muck alone. And yet the Brodies and their students estimate that there’s enough TTX in one newt egg to kill somewhere between 500 and 3700 caddisflies.

You know where this is going. At the evolution meeting, one of their students, Brian Gall, described feeding newt skin to caddisflies both from the central Oregon ponds and from ponds elsewhere without newts. The newt-free caddisflies would happily munch on newt skin from which all the TTX was removed. But if there was more than a trace TTX in the skin, they refused to eat. The caddisflies that fed on newt eggs, on the other hand, would eat the most toxic skin Gall could provide.

It appears that the caddisflies have evolved much like the garter snakes. In ponds where rough-skinned newts lived, the caddisflies have evolved defenses against TTX. In fact, Gall reported, the caddisflies appear to put the snakes to shame. Evolved snakes are 34 times more resistant to TTX than vulnerable ones. The caddisflies have increased their resistance 175 times.

It’s not clear whether the caddisflies and the newts are truly co-evolving, however. The Brodies will have to find out whether adding extra TTX to eggs increases their survival in the presence of caddisflies. Another intriguing possibility arises from their discovery that the caddisflies actually harbor some of the TTX they eat in their tissues for weeks after eating the eggs. Perhaps the caddisflies are stealing the poison to protect themselves, as happens in monarch butterflies eating toxic milkweed.

In other words, this wonderfully deadly story isn’t over yet.

[For more information, see this new paper in Can. J. Zool., and Understanding Evolution, an educational web site. Ed Brodie tells much of the story pre-caddisfly in a chapter of the new book, In The Light of Evolution (full disclosure: I wrote a chapter in it, too, which you can read as a pdf here)]

Image: California Herps

Brian Malow and I talked yesterday about some of my favorite things on the latest episode of Dr. Kiki’s Science Hour–including the evolution odometer. You can watch it on Youtube, or you can head over to Dr. Kiki’s Science Hour site to download the video or audio. (The Skype goes berserk briefly, but we get back on track.)

The Quarterly Review of Biology delivers a rave for The Tangled Bank: An Introduction to Evolution. Daniel McShea of Duke University writes:

This is the first textbook I have seen by a professional science writer. If this is a sort of experiment in textbook publishing, it is a spectacularly successful one…The result is an introduction to the field that is not only accurate and up to date, but—of course—well written. How important is the prose in a textbook? For students, lively versus leaden, or clear versus cryptic, can be the difference between understanding and not, between being turned on to a field and being turned off. For what it is worth, I solicited help for this review from a biologically inclined high school student, who read a few chapters and reported it to be both clear and engaging….In summary, this is an excellent textbook, one that ought to be—and will be, I predict—widely adopted.

Last summer I wrote in the New York Times about a controversy over one of the most influential concepts in the recent history of evolutionary biology. Known as inclusive fitness, it basically says that helping relatives can be a good way to pass on your genes, because they’ve got your genes too.

In August, Nature published a lengthy paper by Martin Nowak, E.O. Wilson, and Corina E. Tarnita in which they argued that inclusive fitness was mathematically flawed and basically superfluous. I had no trouble finding other scientists who were ready to say all sorts of scathing things about Nowak et al. I’m no fan of ginning up fake debates, but when somebody says, “This paper, far from showing shortcomings in inclusive fitness theory, shows the shortcomings of the authors,” the story writes itself.

Seven months later, Nature has finally published some “Brief Communication Arising” letters from some of these critics. The first letter alone has 137 co-signers.

Their ranks include plenty of major players in the field of evolution (including John Alcock, Tim Clutton-Brock, Stephen Emlen, Paul Sherman, Mary-Jane West Eberhard, and Richard Wrangham). The tenor of the letters is more dignified than the comments I got for my story, but the message is unchanged:

We believe that their arguments are based upon a misunderstanding of evolutionary theory and a misrepresentation of the empirical literature.

The authors of the first letter argue that Nowak et al don’t get inclusive fitness. They claim it needs lots of stringent assumptions, when, in fact, it’s a general theory. They also challenge the idea that inclusive fitness doesn’t provide any more insights into biology. They offer a list of such insights, such as why animals cooperate with each other, why they can act spitefully, and why mothers produce different ratios of males and females. Inclusive fitness has proven particularly useful for addressing last question–what’s known as sex allocation. It explains how the ratio of males to females changes with the density of females, the mortality rate, and many other factors–and it does so for species as varied as mammals, birds, spiders, and plants.

Nowak et al respond to all the criticism and don’t budge in their own stand. They claim that their critics have misinterpreted their own argument. And they claim that sex allocation does not require inclusive fitness. Oddly, though, they never explain why it doesn’t, despite the thousands of papers that have been published on inclusive fitness and sex allocation. They don’t even cite a paper that explains why. They conclude by writing,

Inclusive fitness theory is neither useful nor necessary to explain the evolution of eusociality or other phenomena. It is time for the field of social evolution to move beyond the limitations of inclusive fitness theory.

[Image from Alex Wild]

Last week I wrote in the New York Times about a fascinating new paper in which scientists described a lamp shell embryo that is, in effect, a swimming eyeball. The paper itself, however, comes in two parts. Along with the part on the swimming eyeball, the scientists also described a later stage of the lamp shell embryo in which it developed simple eyes connected to neurons. It’s primitive version of our own eyes that reveals some interesting things about evolution–particularly about the different photoreceptors that evolved over half a billion years ago for sensing light. At the time, I was struck by the fact that this one paper had two newsworthy insights. So I was glad to see PZ Myer takes up the other half of the story in excellent detail over at Pharyngula. Check it out.

Tomorrow’s Science Times section of the New York Times has a special package of articles all about animals–the relationship between humans and the animals we raise, what makes us separate from animals, and so on. I took the opportunity to take a big step back and look at how animals came to be in the first place. The answer–or at least part of it–lies among some weird creatures, such as this tentacled creature that dwells inside snails. Check it out.