I’ve got a story on the cover of the latest issue of Time. It’s about the evolutionary origins of friendship. For a number of scientists, friendship–in a deep sense of the word–is not limited to our own species. The fact that friendship may be a widespread biological phenomenon could help us better understand why it has such a positive effect on our own health.

If you’re interested in the scientific literature, the best way in–and the way I first started to get familiar with it–is this review in the latest issue of Annual Review of Psychology by Dorothy Cheney and Robert Seyfarth, two of the world’s leading primatologists.

One thing that I delve into in the story is the question of just how widespread animal friendship really is. We don’t know, in large part because scientists haven’t done that many long-term field studies on wild animals. When scientists do watch dolphins or baboons for decades, they can see some bonds between unrelated individuals that last for long stretches. (Yet another value that comes from slow-cooked science.) On the other hand, what may look like friendship may just be anthropomorphic projection. In the article, I explain that a lot of cross-species “friendships” may be nothing like the kind seen in, say, chimpanzees. (As for the adorable dogs are on this week’s cover of Time, I note that the evidence about man’s best “friend” is quite thin.)

My story is behind a paywall, so you’ll need to subscribe or pick up a copy at a news stand. For a sense of the piece, here are the first few paragraphs–

Since 1995, John Mitani, a primatologist at the University of Michigan, has been going to Uganda to study 160 chimpanzees that live in the forests of Kibale National Park. Seventeen years is a long time to spend watching wild animals, and after a while it’s rare to see truly new behavior. That’s why Mitani loves to tell the tale of a pair of older males in the Kibale group that the researchers named Hare and Ellington.

Hare and Ellington weren’t related, yet when they went on hunting trips with other males, they’d share prey with each other rather than compete for it. If Ellington reached out a hand, Hare would give him a piece of meat. If one of them got into a fight, the other would back him up. Hare and Ellington would spend entire days traveling through the forest together. Sometimes they’d be side by side. Other times, they’d be 100 yards apart, staying in touch through the foliage with loud, hooting calls. “They’d always be yakking at each other,” says Mitani.

Their friendship—for that’s what Mitani calls it—lasted until Ellington’s death in 2002. What happened next was striking and sad. For all the years that Mitani had followed him, Hare had been a sociable, high-ranking ape. But when Ellington died, Hare went through a sudden change. “He dropped out,” says Mitani. “He just didn’t want to be with anybody for several weeks. He seemed to go into mourning.”

In yesterday’s New York Times, I wrote about a new paper in which scientists report the evolution of single-celled yeast into multicellular snowflake-like “bodies.” Most (but not all) of the experts I contacted for the story had high praise for the study. (It also won an award when it was presented as a talk over the summer at the Society for the Study of Evolution.) Once the story appeared, however, some scientists took to Twitter to express their skepticism. As much as I like Twitter, this is one of the situations where it fails. You can’t have a conversation about genetics, lab strains versus wild types, etc., in 140 character chunks. At least not very satisfying ones.

So here’s what I decided to do last night. I used Storify to collect the comments of Leonid Kruglyak of Princeton and Michael Eisen of Berkeley, and then passed them on to Will Ratcliff, the lead author of the new study. He then responded. Below you’ll find the Storify tweets, and then Ratcliff’s response. Please continue the conversation in the comment thread. (And be sure to download the paper–it’s open access.)

Will Ratcliff responds:

Well, I don’t buy it that yeast are multicellular in nature. Certainly some yeast in nature form small clusters (like strain RM11), but as far as I know, these are the exception to the rule. Most strains isolated in nature are unicellular, or at most, flocculating (which I still count as unicellular but social). [CZ: "Flocculating" refers to the clumps that unrelated yeast cells form when they starve.]

Our yeast are not utilizing ‘latent’ multicellular genes and reverting back to their wild state. The initial evolution of snowflake yeast is the result of mutations that break the normal mitotic reproductive process, preventing daughter cells from being released as they normally would when division is complete. Again, we know from knockout libraries that this phenotype can be a consequence of many different mutations. This is a loss of function, not a gain of function. You could probably evolve a similar phenotype in nearly any microbe (other than bacteria, binary fission is a fundamentally different process). We find that it is actually much harder to go back to unicellularity once snowflake yeast have evolved, because there are many more ways to break something via mutation than fix it. The amazing thing we see is that we rapidly see adaptations to this adaptation. If we select for more rapid settling, snowflake yeast evolve to delay reproduction until the parent is larger, allowing it settle more quickly. We see the evolution of higher rates of apoptosis as a way to regulate the size and number of propagules produced. We show that the transition to multicellularity in yeast is surprisingly easy, and have no reason to suspect it would be any harder in other microbes with a reproductive process similar to yeast.

In the history of life, single-celled microbes have evolved into multicellular bodies at least 25 times. In our own lineage, our ancestors crossed over some 700 million years ago. In tomorrow’s New York Times, I write about a new study in which single-celled yeast evolved into multicellular forms–completely with juvenile and adult forms, different cell types, and the ability to split off propagules like plant cuttings. All this in a matter of weeks. Check it out.

(The paper is not yet online yet, but here’s the reference: “Experimental evolution of multicellularity,” William C. Ratcliff, R. Ford Denison, Mark Borrello, and Michael Travisano. Proceedings of the National Academy of Sciences. http://www.pnas.org/cgi/doi/10.1073/pnas.1115323109 )

Update: Here’s a Twitter-Storify-blog follow up on some reactions to the study.

Each year, literary agent and science salonista John Brockman poses a question about science and gets a slew of answers from scientists, writers, and other folks. This year’s question is

WHAT IS YOUR FAVORITE DEEP, ELEGANT, OR BEAUTIFUL EXPLANATION?

Brockman got 187 responses, totaling some 126,700 words. A book, you say! Well, if this year is like previous ones, this year’s answers will indeed become a book. But in the meantime, you can browse the answers for yourself, perhaps plucking out those of your favorite people. (Fellow Discover blogger cosmologist Sean Carroll chooses Einstein’s explanation of gravity, for example.)

I found this year’s question particularly thought-provoking. Why is it that we call an equation or a theory “beautiful”? They don’t have pretty hazel eyes. They aren’t desert landscapes. I’m not sure of the answer. Scientific explanations seem to be beautiful if they give sense to confusing complexity in a very short space. Or maybe we just like the feeling we get when we consider how our puny human brains can interpret the universe.

For a lot of physicists, the beauty of an equation seems to be a good hint that it’s probably true. But I’m always a bit suspicious of beauty as a guide to the natural world. A number of contributors selected Darwin’s theory of evolution as their favorite explanation, and there’s no doubt that’s both beautiful and true. But there have been some wonderfully beautiful accounts of the natural world that have proven awesomely wrong. I was reminded of this fact while working on a new version of my evolution textbook (this one’s for biology majors). I was re-researching how scientists first came to appreciate the vast age of our planet, and realized it was a bit more complicated than I had previously appreciated. So that’s what I chose as my answer, which I’m reprinting here in full:

A Hot Young Earth: Unquestionably Beautiful and Stunningly Wrong

Around 4.567 billion years ago, a giant cloud of dust collapsed in on itself. At the center of the cloud our Sun began to burn, while the outlying dust grains began to stick together as they orbited the new star. Within a million years, those clumps of dust had become protoplanets. Within about 50 million years, our own planet had already reached about half its current size. As more protoplanets crashed into Earth, it continued to grow. All told, it may have taken another fifty million years to reach its full size—a time during which a Mars-sized planet crashed into it, leaving behind a token of its visit: our Moon.

The formation of the Earth commands our greatest powers of imagination. It is primordially magnificent. But elegant is not the word I’d use to describe the explanation I just sketched out. Scientists did not derive it from first principles. There is no equivalent of E=mc2 that predicts how the complex violence of the early Solar System produced a watery planet that could support life.

In fact, the only reason that we now know so much about how the Earth formed is because geologists freed themselves from a seductively elegant explanation that was foisted on them 150 years ago. It was unquestionably beautiful, and stunningly wrong.

The explanation was the work of one of the greatest physicists of the nineteenth century, William Thompson (a k a Lord Kelvin). Kelvin’s accomplishments ranged from the concrete (figuring out how to lay a telegraph cable from Europe to America) to the abstract (the first and second laws of thermodynamics). Kelvin spent much of his career writing equations that could let him calculate how fast hot things got cold. Kelvin realized that he could use these equations to estimate how old the Earth is. “The mathematical theory on which these estimates are founded is very simple,” Kelvin declared when he unveiled it in 1862.

At the time, scientists generally agreed that the Earth had started out as a ball of molten rock and had been cooling ever since. Such a birth would explain why rocks are hot at the bottom of mine shafts: the surface of the Earth was the first part to cool, and ever since, the remaining heat inside the planet has been flowing out into space. Kelvin reasoned that over time, the planet should steadily grow cooler. He used his equations to calculate how long it should take for a molten sphere of rock to cool to Earth’s current temperature, with its observed rate of heat flow. His verdict was a brief 98 million years.

Geologists howled in protest. They didn’t know how old the Earth was, but they thought in billions of years, not millions. Charles Darwin—who was a geologist first and then a biologist later—estimated that it had taken 300 million years for a valley in England to erode into its current shape. The Earth itself, Darwin argued, was far older. And later, when Darwin published his theory of evolution, he took it for granted that the Earth was inconceivably old. That luxury of time provided room for evolution to work slowly and imperceptibly.

Kelvin didn’t care. His explanation was so elegant, so beautiful, so simple that it had to be right. It didn’t matter how much trouble it caused for other scientists who would ignore thermodynamics. In fact, Kelvin made even more trouble for geologists when he took another look at his equations. He decided his first estimate had been too generous. The Earth might be only 10 million years old.

It turned out that Kelvin was wrong, but not because his equations were ugly or inelegant. They were flawless. The problem lay in the model of the Earth to which Kelvins applied his equations.

The story of Kelvin’s refutation got a bit garbled in later years. Many people (myself included) have mistakenly claimed that his error stemmed from his ignorance of radioactivity. Radioactivity was only discovered in the early 1900s as physicists worked out quantum physics. The physicist Ernst Rutherford declared that the heat released as radioactive atom broke down inside the Earth kept it warmer than it would be otherwise. Thus a hot Earth did not have to be a young Earth.

It’s true that radioactivity does give off heat, but there isn’t enough inside the planet is to account for the heat flowing out of it. Instead, Kelvin’s real mistake was assuming that the Earth was just a solid ball of rock. In reality, the rock flows like syrup, its heat lifting it up towards the crust, where it cools and then sinks back into the depths once more. This stirring of the Earth is what causes earthquakes, drives old crust down into the depths of the planet, and creates fresh crust at ocean ridges. It also drives heat up into the crust at a much greater rate than Kelvin envisioned.

That’s not to say that radioactivity didn’t have its own part to play in showing that Kelvin was wrong. Physicists realized that the tick-tock of radioactive decay created a clock that they could use to estimate the age of rocks with exquisite precision. Thus we can now say that the Earth is not just billions of years old, but 4.567 billion.

Elegance unquestionably plays a big part in the advancement of science. The mathematical simplicity of quantum physics is lovely to behold. But in the hands of geologists, quantum physics has brought to light the glorious, messy, and very inelegant history of our planet.

[Post-script: Thanks to responses from readers, I can see how this essay is confusing. I added some passages from the papers I cite below down in the comment thread, which I hope can clear things up a bit.]

[Update: For an up-to-date review of the age and formation of the Earth, see this paper [abstract, free pdf] For a great look at Kelvin’s work, see this piece in American Scientist or the more technical paper on which it was based (free pdf).]

[Image: Photo by Hawaiian Sea - http://flic.kr/p/8AyKnC via Creative Commons]

Cancer evolves. Those two words may sound strange together. Sure, birds evolve. Bacteria evolve. But cancer? The trouble arises from the fact that cancers, unlike birds and bacteria, are not free-living organisms. They start out as cells inside a person’s body and stay there, until they’re either wiped out or the person dies.*

Yet the same forces that drive the evolution of free-living organisms can also drive cancer cells to become more aggressive and dangerous. Evolution becomes our inner foe if mutations disable a cell’s self-restraint. The cell multiplies. Sometimes a new mutation arises in its descendants. If the mutations allow the cancer to grow faster, the cells carrying it will take over the population of cancerous cells. Natural selection and other processes that drive evolution on the outside start driving it on the inside.

Like so many other scientists, researchers who study cancer evolution have jumped on new technology for sequencing genomes on the cheap. They’re now starting to publish fine-grained histories of the disease, tracking individual mutations as they arise and spread. Nature has just published a fine example of this new research. I particularly appreciated the informative pictures they came up with to accompany the paper, one of which I’ve included here. You can click on the picture for a bigger version. And below the picture, I’ll explain what it means.

In the new paper, Li Ding and colleagues at Washington University describe a study they carried out on eight people suffering from acute myeloid leukemia (AML), a disease of the immune system. In people with AML, stem cells in the bone marrow that would normally turn into white blood cells instead become cancerous. Treatments include bone marrow transplants and chemotherapy. Unfortunately, AML has a nasty way of bouncing back from chemotherapy, and the drugs become useless to stop it. As a result, a lot of people who seem at first to be in remission eventually die of the cancer.

The Washington University scientists reconstructed the history of the cancer in each patients by sequencing genomes from a number of cells. To determine the normal, original genome, they sequenced DNA from a healthy skin cell. They then sequenced genomes from cancer cells taken from the patients when they were first diagnosed. And then they looked at genomes of cancer cells that emerged after the patients relapsed. From this survey, they came up with a catalog of new mutations that emerged over the course of the cancer. They could then go back into the blood samples and estimate what fraction of the cancer cells had a given mutation at a given point in time.

This figure illustrates the sad chronicle of one particular woman they studied. When she was in her late 50s, she suddenly came down with a sore throat and began to bruise easily. A bone marrow biopsy confirmed she has AML. She got chemotherapy, and then a stem cell transplant. Although she seemed to go into complete remission, the cancer returned 11 months after her diagnosis. The chemotherapy drugs that had previously been so effective now could not stop the cancer. Other drugs failed, too. Two years after her diagnosis, she died.

On the left of the figure, the cancer begins. A single stem cell mutated and became the founder of the cancerous lineage. we start with normal cells. (The cell is dark, and the grey dot marks its original mutation. HSC stands for hematopoietic stem cells).

The cancer cells grew in number, and as they did, they accumulated a lot of mutations, some of which are listed in the figure next to the star. All of these mutations, one after the other, took over the entire population of cells–a signature of natural selection. When the woman went to her doctor, however, the cancer had diversified into a number of different lineage, each carrying additional, distinctive mutations. Over half of the cells belonged to a lineage marked here in purple, known as cluster 2. Cluster 3, marked in yellow, was made up cells with a separate set mutations. And from within Cluster 3 emerged yet another lineage–Cluster 4, marked in orange. The dots in each circle show the sets of mutations that accumulated in each cluster.

The chemotherapy knocked down all the clusters of cancer cells to such low numbers that doctors couldn’t find them any more. But they were still there. And when exposed to chemotherapy drugs, the most successful cluster was not the one that had been most successful back when the cancer was diagnosed. It was the relatively rare Cluster 4. Apparently, it had mutations that made it better able to withstand the chemotherapy drugs. Some its descendants later picked up new mutations, which enabled them to reproduce quickly and take over the cancer population, as they resisted new chemotherapy drugs as well.

“The AML genome in an individual patient is clearly a ‘moving target,’” the scientists right conclude. “Eradication of the founding clone and all of its subclones will be required to achieve cures.” Easier said than done, of course. The parallels between this research and studies on antibiotic resistance in bacteria are sobering. But at least now we’re starting to see what kind of evolutionary challenge we’re really up against.

(*For one very cool exception to this rule, consider the case of Tasmanian devil facial tumors, which travel from devil to devil. They evolve too, though.)

This is a story of about how the parts of a puzzle locked into place 800 million years ago. The puzzle is an ion pump that you can find in any mushroom, mold, or yeast. I’ve reproduced a picture of it here.

Fungus cells, like our own cells, have lots of little pouches inside of them for carrying out special kinds of chemical reactions. In order for those reactions to work, there have to be a lot of positively-charged protons inside the pouches. To get those protons into the pouches, ion pumps like this one force them through membranes.

This pump (which is is offically known as a vacuolar ATPase complex) is a wonderfully complex collection of proteins. They fit together elegantly, and they cooperate to get this vital job done. One particularly cool feature of this pump is the ring lodged in the pouch’s membrane, where it spins around like a wheel. The ring is made up of six proteins–four copies of a protein called Vma3, and a single copy of two other proteins called Vma11 and Vma16–that lock together. If a mushroom can’t make all three types of proteins, its pump won’t work. And without a pump, it’s a dead mushroom. Simple as that.

Joe Thornton, a biologist at the University of Oregon, and his colleagues wondered how this pump came to be. Readers of the Loom may recall a couple previous posts I’ve written about Thornton’s work. He traces the molecular history of life by resurrecting proteins from hundreds of millions of years ago and playing around with them to figure out how they work. This week in Nature, Thornton and his colleagues describe the history of the fungus ion pump. It’s the first time they’ve reconstructed the history of such a molecular “machine” this way. It’s also a useful lesson in the ways complex things evolve–especially things that seem so complex that it’s hard to imagine how they could have evolved step by step from something simpler.

The closest major group of species to fungi are animals. Like fungi, we have vacuolar ATPase complexes in our cells. But they’re different. Instead of three types of proteins in the ring, we only have two types–five copies of Vma3, and one of Vma16. When it comes to ion pumps, at least, we are pretty primitive compared to mushrooms.

The scientists compared the genes for these ring proteins to other genes in order to reconstruct their evoluationary history. They discovered that Vma11, the ring protein unique to the fungi, and Vma3 are closely related. At some point after the ancestors of fungi branched off from the ancestors of animals, an ancestral ring protein duplicated, forming the Vma3 and Vma11 proteins in fungi. Both of the proteins evolved a lot after the duplication. Thornton estimates that 25 amino acids changed between the ancestral protein and Vma3 in fungi, and 31 changed on the way to Vma11.

By comparing Vma3 and Vma11 in yeast, Thornton and his colleagues were able to infer the structure of their ancestral protein. They then created that long-vanished protein (which they dupped Anc.3-11) and ran an experiment to see how it worked 800 million years ago.

To run their experiment, the scientists first shut down the Vma3 and Vma11 genes in yeast cells. Normally, this would stop the yeast from growing. But then they inserted the Anc.3-11 gene into the yeast. The yeast build a two-protein ring instead of its normal three-protein ring, and did just fine with them. Thornton and his colleagues then created yeast strains with just Vma3 shut down. The yeast could combine Vma11 and Vma16 with Anc.3-11 to make a working ring. The same success occurred when they only shut down Vma11.

Based on experiments such as these, Thornton has developed a hypothesis to explain how the ring evolved. This picture illustrates the steps. The ancestral ring in the common ancestor of animals and fungi is shown on the right. It only has two types of proteins. Green is the ancestral form of Vma3 and 11, and red is the ancestral Vma16. The black squares, circles, and triangles represent parts of the proteins that can only lock onto certain parts of other proteins (represented by the matching recesses). As you can seen, the green protein (the ancestor of Vma3 and Vma11) is versatile, able to lock onto several different proteins.

Animals have the same basic ring. In fungi, on the other hand, some important changes happened. First, Anc.3-11 duplicated. (Vma11 is shown in yellow.) Then the links between the proteins changed. None of the proteins gained any new functions, however. Instead, simple mutations caused them to lose an interface. The red dots on the blue and yellow fungal protein show where these interfaces disappeared. These mutations robbed the proteins of  their former versatility. As a result, the ring now only fits together if all three types of proteins are present in one particular arrangement.

You might think that life gets more complex as it evolves new features. Our eye can form sharp images, for example, but in order to do so, it first had to evolve a cavity, a pinhole opening, and a lens. In the case of this ring, however, Thornton has found just the opposite. Its simpler ancestor was made up of more versatile proteins. As the proteins duplicated and degenerated, their arrangement became more complicated. No one can say yet how often this kind of evolution happened. We’ll have to wait for some more molecular time travel for an answer.

In 1494, King Charles VIII of France invaded Italy. Within months, his army collapsed and fled. It was routed not by the Italian army but by a microbe. A mysterious new disease spread through sex killed many of Charles’s soldiers and left survivors weak and disfigured. French soldiers spread the disease across much of Europe, and then it moved into Africa and Asia. Many called it the French disease. The French called it the Italian disease. Arabs called it the Christian disease. Today, it is called syphilis.

I’ve been intrigued by the murky history of syphilis for a few years now. The text above is from the start of an article I wrote for Science in 2008. At the time, scientists were split between two explanations for sudden appearance of syphilis at the end of the fifteenth century. According to one, it was caused by bacteria that had evolved in the New World and were brought back to Europe by Columbus’s crew. But other researchers found many skeletons with signs of syphilis in Europe, Africa, and Asia that appeared to have been from long before Columbus’s voyage. They argued that it must have started in the Old World, perhaps before people even left for the New World some 15,000 years ago.

As I explained in the article, one way to test these hypotheses is to survey the evolution of the bacteria. A group of researchers based at Emory University came across bacteria infecting Indians in Guyana that was genetically close, but not identical, to syphilis. They suggested syphilis had evolved in the New World from a common ancestor of both pathogens. Columbus’s crew may have picked it up when they visited the New World and then brought it home to Europe. Unfortunately, by the time doctors had gotten the bacteria from the jungles of Guyana to a laboratory where it could be analyzed, the DNA was in bad shape, so they couldn’t come to a firm conclusion.

Recently, I caught up with one of the scientists on the team, Kristin Harper, who is now at Columbia University. She didn’t have any new genetic results to talk about, unfortunately, although she may before long. In the meantime, she pointed me to a new review she has published in the Yearbook of Physical Anthropology. She and her colleagues took a look at the bones that scientists have pointed to as evidence for the antiquity of syphilis in both the New and Old World, and passed judgment about just how good the evidence was that they did, indeed, have syphilis, and not some other disease that can deform bone. The scientists also took a close look at the dating of the bones, since the timing of syphilis’s origin is so crucial to the entire debate.

The trouble with a lot of past research, Harper says, is that scientists have come up with new ways to diagnose syphilis in ancient bones without offering good evidence that their criteria are good. “Paleopathology is kind of the wild west of science, in that the ‘rules’ are still in their infancy,” Harper said. “We set ourselves the challenge of using only evidence-based diagnostic criteria in this paper and tried to be similarly stringent about dating.”

The scientists looked at 54 reports from both hemispheres. Most of the Old World bones failed to meet at least one of the standard requirements for a diagnosis of syphilis, such as distinctive pits on the skull or swelling in the long bones of the arms and legs. But when they looked at the Old World bones that had been dated to before 1492 that did make the grade, they ended up throwing all of those bones out, too. The evidence that these Old World bones were from before 1492 turned out to be weak. They tended to come from coastal regions, where people eat lots of fish. Fish are full of carbon from deep in the ocean, which has a different balance of isotopes than that found on the land. The ocean carbon gets into the bones of coastal people, where it can throw off estimates of their age by centuries. A close examination of these coastal Old World bones led the Emory scientists to conclude that they belonged to Europeans who died shortly after Columbus’s voyage.

“In contrast,” Harper told me, “we found definite cases of treponemal disease [syphilis] hailing from the New World that stretched back thousands and thousands of years.”

Harper and her colleagues conclude that there’s no good evidence for syphilis in the Old World, and plenty in the New World. They continue to argue that syphilis traveled east across the Atlantic.

It’s intriguing if Harper turns out to be right. Europeans brought smallpox and other pathogens to the New World which decimated its residents. Syphilis, it seems, is one pathogen that went the other way.

[Image of Columbus voyage: Wikipedia]

[Update, 12/19 7 pm: Some of the comments prompted me to edit this piece for clarity.]

Long before Darwin published The Origin of Species, there was talk of evolution. The more acquainted naturalists became with the major groups of animals, the gaps between them grew smaller. Once it seemed as if mammals were profoundly different than other vertebrates, for example. And then European explorers encountered the platypus, a mammal that laid eggs. Perhaps the major groups of animals had not been separately created, some naturalists suggested. Perhaps life had changed over time.

In 1837, a profoundly paradoxical creature was shipped from West Africa to London, packed in clay. It was destined for Richard Owen, the greatest British anatomist of his age. He picked away the clay, to reveal a creature that looked like a fish. It has a knife-shaped body, gills, and fins. “If indeed the species had been known only by its skeleton,” Owen wrote, “no one could have hesitated in referring it to the class of Fishes.”

But inside its body, Owen found what he could only call lungs. Its whisker-like fins had a chains of bones that faintly resembled arms. Owen was a fierce opponent of all the transformationists of his day, and he was determined to find a way to push this creature–what Owen called Lepidosiren and what we today commonly call a lungfish–to one side of the divide or the other. He finally found an antidote to evolution in its nose.

Owen’s examination led him to conclude that the nostrils of the lungfish did not connect to its mouth. They seemed to end in a blind pouch. That was a hallmark of fish, and the trait banished lungfish from the tetrapods–the land vertebrates such as reptiles, birds, and mammals. “According to this test, Lepidosiren is a Fish…simply by its nose,” he wrote.

As I write in my book At the Water’s Edge, Owen turned out to be wrong. In 1860, a year after Darwin published his theory of evolution, an Irish anatomist named Robert M’Donnel discovered a passageway from the lungfish’s nose to its mouth. It was, he concluded, a transitional creatures, with some traits from our fishy past mixed with traits also found in tetrapods. “I know of no animal more calculated leading to the adoption of the theory of Darwin, than the Lepidosiren,” he wrote.

Since then, scientists have amassed an overwhelming amount of evidence that lungfish are close kin to tetrapods. Their kinship is inscribed in their DNA, for example: genetic tests consistently show that of the 30,000-odd species of fish, lungfish are the closest (or among the closest) relatives to tetrapods.

On the other hand, we shouldn’t rush to the conclusion that the lungfish is a living fossil, a snapshot of our own ancestry. Lungfish and tetrapods share a common ancestor that lived some 400 million years ago. Since then, the lungfish lineage has gone through drastic changes. Some 350 million years ago, rivers and coastal waters were loaded with a diversity of lungfishes, including massive predators the size of sailboats. Today, lungfish are a whisper of that former glory, a few species eking out an existence in Australia, Brazil, and Africa. The living lungfishes are different from each other in some important ways. The lungfish in Africa have wispy fins and dig into the mud to survive droughts. The lungfish of Australia have stout lobe-shaped fins and never escape droughts in the mud.

Once scientists can sort out what’s new about lungfishes, they can then take a look at what’s old. And therein lie some intriguing clues about our own origins. Today, scientists at the University of Chicago published a study of lungfish that sheds light on the origin of one of the most essential behaviors for a tetrapod: the ability to walk. In their own weird way, lungfish can walk, too.

Tetrapods walk in many different ways. Lions race, sloths lumber, salamanders squirm. But all tetrapod walks are built on the same foundation. A tetrapod typically alternates its forelegs and hind legs, pushing each limb against the ground to propel itself forward. Early tetrapods bent their trunks from side to side as they moved, and amphibians like salamanders still do today. Other tetrapods modified their walks; most mammals keep their trunk from bowing out to the sides, instead flexing it up and down.

That’s a far cry from the typical way fishes move. They propel themselves forward through the water with their tails, adjusting their fins to help them control their movements. They mainly flap their pectoral fins (which correspond to our arms). One glaring exception to this kind of locomotion is a deep-water fish known as the coelacanth. It swims by alternating its lobe-shaped fins. And it just so happens that the coelacanth is the only other aquatic animal that shares the same close kinship to tetrapods as lungfish.

Some researchers who have observed lungfishes in the wild have noticed that they also seem to move their fins in an alternating pattern. To see whether that was actually true, Heather King of the University of Chicago and her colleagues have been filming lungfish in lab tanks and then analyzing their movement on computers.

King found that the lungfishes regularly moved around their tank by pushing off the bottom with their pelvic fins (which correspond to hind legs). They alternated between the fins in a walk-like pattern, sometimes switching to a bounding, synchronous gait. With each step, the lungfishes lifted their bodies up and forward, much like tetrapods do while walking. (The movie below shows a few samples of her footage.)

It’s pretty remarkable that lungfish can come so close to walking. They have no pelvis to help them transmit the force they generate pushing off the bottom of the tank to the rest of their body. Their their fins contain thin chains of bones, with no foot or ankle. King’s research suggests that an animal doesn’t need all that much tetrapod anatomy to walk.

This discovery offers a new way to interpret some enigmatic track marks dating back to the time when the first tetrapods evolved. These trackways seem to have been formed by a limbed animal with an alternating gait. But there are no toe marks preserved with them. It’s possible, King suggests, that early relatives of tetrapods made them, with limbs as simple as those of lungfishes.

It also underscores one of the most counterintuitive facts about how our ancestors evolved into land-walking vertebrates. Our limbs are so well-adapted for moving around on land that it’s tempting to think that they must have first evolved expressly for that purpose. Indeed, for much of the 1900s, many scientists believed tetrapods evolved when fish had to crawl from pond to pond to survive droughts. It’s clear, however, that many of the key elements of a walking body–such as limbs that an animal could move in an alternating gait to push itself forward–evolved long before our ancestors came on land. The lungfish, M’Donnel might say, is more calculated than ever to lead to the adoption of the theory of Darwin.

King et al, Behavioral evidence for the evolution of walking and bounding before terrestriality in sarcopterygian fishes. PNAS. http://www.pnas.org/cgi/doi/10.1073/pnas.1118669109

[Photo by Joel Abroad Flickr/Creative Commons]

The New York Times has launched a series called Profiles in Science. When I was invited to join the undertaking, I proposed writing about the Harvard psychologist Steven Pinker. I had run into Pinker at the World Science Festival in June, and he had told me about his next book, The Better Angels of Our Nature, which was due out in the fall. In the 800+ page tome, Pinker argues that rates of human violence have been crashing for millennia, and he offers psychological explanations for the fall.

I’ve followed Pinker’s work since I first came across his 1994 book, The Language Instinct. In the wake of the book’s success, he quickly became a leading exponent of evolutionary psychology, coming out swinging against its critics such as Stephen Jay Gould. When Pinker described his book to me, I was intrigued. I wondered how someone who argued that human nature was shaped long ago by natural selection would end up arguing that human nature–or at least human experience–is now changing rapidly for the better. But there were other things I was wondering–how, for example, does a writer of massive books about human nature live inside the same body as an expert on irregular verbs?

So I headed up to Cambridge to ask a bunch of questions, out of which a profile emerged. You can read it in tomorrow’s Times, or on their web site.

At the site, you can also watch a video interview with Pinker from NYT senior producer Thomas Lin.

We know that our species is unique, but it can be surprisingly hard to pinpoint what exactly makes us so. The fact that we have DNA is not much of a mark of distinction. Several million other species have it too. Hair sets us apart from plants and mushrooms and reptiles, but several thousand other mammals are hairy, too. Walking upright is certainly unusual, but it doesn’t sever us from the animal kingdom. Birds can walk on two legs, after all, and their dinosaur ancestors were walking bipedally 200 million years ago. Our own bipedalism–like much of the rest of our biology–has deep roots. Chimpanzees, whose ancestors diverged from our own some seven million years ago, can walk upright, at least for short distances.

If looking for human uniqueness on the outside is difficult, is it any easier to look on the inside–in particular, at our mental lives? There’s no doubt that our minds allow us to do things that even our great ape relatives cannot. For one thing, we can represent the world symbolically in our heads, and we can use words to communicate that symbolic thought to one another. Yet we can sometimes find surprising links between our own mental lives and those of other animals. We’re very good at making and using tools, but that doesn’t mean other animals can’t do so as well. Thinking about the future may seem like a quintessentially human activity, but there’s some evidence that some bird species can travel forward in time, too.

Yet even as scientists find more links between our own faculties and those of other animals, some continue to stand out. And their rugged distinctiveness makes them all the more interesting. One of the most distinctive of all is, to me at least, the most surprising: teaching. (more…)

When the Society for Neuroscience gets together for their annual meeting each year, a city of scientists suddenly forms for a week. This year’s meeting has drawn 31,000 people to the Washington DC Convention Center. The subjects of their presentations range from brain scans of memories to the molecular details of disorders such as Parkinson’s and autism. This morning, a scientist named Svante Paabo delivered a talk. Its subject might make you think that he had stumbled into the wrong conference altogether. He delivered a lecture about Neanderthals.

Yet Paabo did not speak to an empty room. He stood before thousands of researchers in the main hall. His face was projected onto a dozen giant screens, as if he were opening for the Rolling Stones. When Paabo was done, the audience released a surging crest of applause. One neuroscientist I know, who was sitting somewhere in that huge room, sent me a one-word email as Paabo finished: “Amazing.”

You may well know about Paabo’s work. In August, Elizabeth Kolbert published a long profile in the New Yorker. But he’s been in the news for over fifteen years. Like many other journalists, I’ve followed his work since the mid-1990s, having written about pieces of Paabo’s work in newspapers, magazines, and books. But it was bracing to hear him bring together the scope of his research in a single hour–including new experiments that Paabo’s colleagues are presenting at the meeting. Simply put, Paabo has changed the way scientists study human evolution. Along with fossils, they can now study genomes that belonged to people who died 40,000 years ago. They can do experiments to see how some of those individual genes helped to make us human. During his talk, Paabo used this new research to sketch out a sweeping vision of how our ancestors evolved uniquely human brains as they swept out across the world.

Before the 1990s, scientists could only study the shape of fossils to learn about how we evolved. A million years ago, the fossil record contained evidence of human-like creatures in Europe, Asia, and Africa. Roughly speaking, the leading hypotheses for how those creatures became Homo sapiens came in two flavors. Some scientists argued that all the Old World hominins were a single species, with genes flowing from one population to another, and together they evolved into our species. Others argued that most hominin populations became extinct. A single population in Africa evolved into our species, and then later spread out across the Old World, replacing other species like Neanderthals in Europe.

It was also possible that the truth was somewhere in between these two extremes. After our species evolved in Africa, they might have come into contact with other species and interbred, allowing some DNA to flow into Homo sapiens. That flow might have been a trickle or a flood.

As scientists began to build a database of human DNA in the 1990s, it became possible to test these ideas with genes. In his talk, Paabo described how he and his colleagues managed to extract some fragments of DNA from a Neanderthal fossil–by coincidence, the very first Neanderthal discovered in 1857. The DNA was of a special sort. Along with the bulk of our genes, which are located in the nucleus of our cells, we also carry bits of DNA in jellybean-shaped structures called mitochondria. Since there are hundreds of mitochondria in each cell, it’s easier to grab fragments of mitochondrial DNA and assemble them into long sequences. Paabo and his colleagues used the mutations in the Neanderthal DNA, along with those in human and chimpanzee DNA, to draw a family tree. This tree splits into three branches. The ancestors of humans and Neanderthals branch off from the ancestors of chimpanzees 5-7 million years ago, and then humans and Neanderthals branch off in the last few hundred thousand years. If humans carried mitochondrial DNA from Neanderthals, you’d expect Paabo’s fossil genes to be more similar to some humans than others. But that’s not what he and his colleagues found.

Paabo and his colleagues then pushed forward and began to use new gene-sequencing technology to assemble a draft of the entire Neanderthal genome. They’ve gotten about 55% of the genome mapped, which is enough to address some of the big questions Paabo has in mind. One is the question of interbreeding. Paabo and his colleagues compared the Neanderthal genome to genomes of living people from Africa, Europe, Asia, and New Guinea. They discovered that people out of Africa share some mutations in common with Neanderthals that are not found in Africans. They concluded that humans and Neanderthals must have interbred after our species expanded from Africa, and that about 2.5% of the genomes of living non-Africans comes from Neanderthals.

This pattern could have arisen in other ways, Paabo granted. The ancestors of Neanderthals are believed to have emerged from Africa hundreds of thousands of years ago and spread into Europe. Perhaps the humans who expanded out of Africa came from the birthplace of Neanderthals, and carried Neanderthal-like genes with them.

But Paabo doubts this is the case. One way to test these alternatives is to look at the arrangement of our DNA. Imagine that a human mother and Neanderthal father have a hybrid daughter. She has two copies of each chromosome, one from each species. As her own eggs develop, however, the chromosome pairs swap some segments. She then has children with a human man, who contributes his own human DNA. In her children, the Neanderthal DNA no longer runs the entire length of chromosomes. It forms shorter chunks. Her children then have children; her grandchildren have even shorter chunks.

Paabo described how David Reich of Harvard and other scientists measured the size of the chunks of Neanderthal DNA in people’s genomes. They found that in some of the Europeans they studied, the Neanderthal chunks were quite long. Based on their size, the scientists estimated that the interbreeding happened between 37,000 and 86,000 years ago. (This research is still unpublished, but Reich discussed it at a meeting this summer.)

The success with the Neanderthal genome led Paabo to look for other hominin fossils that he could grind up for DNA. DNA probably can’t last more than a few hundred thousand years before degrading beyond recognition, but even in that window of time, there are plenty of interesting fossils to investigate. Paabo hit the jackpot with a tiny chip from the tip of a 40,000-year-old pinky bone that was found in a Siberian cave called Denisova. The DNA was not human, nor Neanderthal. Instead, it belonged to a distant cousin of Neanderthals. And when Paabo and his colleagues compared the Denisovan DNA to human genomes, they found some Denisovan genes in the DNA of their New Guinea subject. Mark Stoneking, Paabo’s colleague at Max Planck, and other scientists have expanded the comparison and found Denisovan DNA in people in Australia and southeast Asia.

Paabo then offered a scenario for human evolution: about 800,000 years ago, the ancestors of Neanderthals and Denisovans diverged from our own ancestors. They expanded out of Africa, and the Neanderthals swept to the west into Europe and the Denisovans headed into East Asia. Paabo put the date of their split about 600,000 years ago. The exact ranges of Neanderthal and Denisovans remain fuzzy, but they definitely lived in Denisova at about the same time 50,000 years ago, given that both hominins left bones in the same cave.

Later, our own species evolved in Africa and spread out across that continent. Humans expanded out of Africa around 100,000 years ago, Paabo proposed. (I’m not sure why he gave that age, instead of a more recent one.) Somewhere in the Middle East, humans and Neanderthals interbred. As humans continued to expand into Europe and Asia, they took Neanderthal DNA with them. When humans got to southeast Asia, they mated with Denisovans, and this second addition of exotic DNA spread through the human population as it expanded. Neanderthals and Denisovans then became extinct, but their DNA lives on in our bodies. And Paabo wouldn’t be surprised if more extinct hominins turn out to have donated DNA of their own to us.

Paabo sees these results as supporting the replacement model I described earlier–or, rather, a “leaky replacement” model. If humans and other hominins had been having lots of sex and lots of kids, we’d have lots more archaic DNA in our genomes.

Now that scientists know more about the history of our genome, they can start tracking individual genes. When I first wrote about this interbreeding work last year for the New York Times, I asked Paabo if there were any genes that humans picked up from interbreeding that made any big biological difference. He didn’t see any evidence for them at the time. But at the meeting, he pointed to a new study of immune genes. One immune gene appears to have spread to high frequency in some populations of Europeans and Asians, perhaps because it provided some kind of disease resistance that benefited them.

The history of other genes is just as interesting. Some of our genes have mutations also found in Neanderthals and Denisovans, but not in chimpanzees. They must have evolved into their current form between 5 million and 800,000 years ago. Other genes have mutations that are found only in the human genome, but not in those of Neanderthals and Denisovans. Paabo doesn’t have a complete list yet, since he’s only mapped half the Neanderthal genome, but the research so far suggests that the list of new features in the human genome will be short. There are only 78 unique human mutations that changed the structure of a protein. Paabo can’t yet say what these mutations did to our ancestors. Some of the mutations alter the address labels of proteins, for example, which let cells know where to deliver a protein once they’re created. Paabo and his colleagues have found that the Neanderthal and human versions of address labels don’t change the delivery.

Other experiments Paabo and his colleagues have been running have offered more promising results. At the talk, Paabo described some of his latest work on a gene called FoxP2. Ten years ago, psychologists discovered that mutations to this gene can make it difficult for people to speak and understand language. (Here’s a ten-year retrospective on FoxP2 I wrote last month in Discover.) Paabo and his colleagues have found that FoxP2 underwent a dramatic evolutionary change in our lineage. Most mammals have a practically identical version of the protein, but ours has two different amino acids (the building blocks of proteins).

The fact that humans are the only living animals capable of full-blown language, and the fact that this powerful language-linked gene evolved in the human lineage naturally fuels the imagination. Adding fuel to the fire, Paabo pointed out that both Neanderthals and Denisovans had the human version of FoxP2. If Neanderthals could talk, it would be intriguing that they apparently couldn’t paint or make sculptures or do other kinds of abstract expressions that humans did. And if Neanderthal’s couldn’t talk, it would be intriguing that they already had a human version of FoxP2. As scientific mysteries go, it’s a win-win.

From a purely scientific point of view, the best way to investigate the evolution of FoxP2 would be to genetically engineer a human with a chimpanzee version of the gene and a chimpanzee with a human version. But since that’s not going to happen anywhere beyond the Island of Doctor Moreau, Paabo is doing the second-best experiment. He and his colleagues are putting the human version of FoxP2 into mice.

The humanized mice don’t talk, alas. But they do change in many intriguing ways. The frequency of their ultrasonic squeaks changes. They become more cautious about exploring new places. Many of the most interesting changes happen in the brain. As I wrote in my Discover column, Paabo and his colleagues have found changes in a region deep in the brain called the striatum. The striatum is part of a circuit that lets us learn how to do new things, and then to turn what we learn into automatic habits. A human version of FoxP2 makes neurons in the mouse striatum sprout more branches, and those branches become longer.

Paabo’s new experiments are uncovering more details about how human FoxP2 changes the mice. Of the two mutations that changed during human evolution, only one makes a difference to how the striatum behaves. And while that difference may not allow mice to recite Chaucer, they do change the way they learn. Scientists at MIT, working with Paabo, have put his mice into mazes to see how quickly they learn how to find food. Mice with human FoxP2 develop new habits faster than ones with the ordinary version of the gene.

So for now, Paabo’s hypothesis is that a single mutation to FoxP2 rewired learning circuits in the brain of hominins over 800,000 years ago. Our ancestors were able to go from practice to expertise faster than earlier hominins. At some point after the evolution of human-like FoxP2, our ancestors were able to use this fast learning to develop the quick, precise motor control required in our lips and tongues in order to speak.

I think what made Paabo’s talk so powerful for the audience was that he was coming from a different world–a world of fossils and stone tools–but he could talk in the language of neuroscience. As big as the Society for Neuroscience meetings can be, Paabo showed that it was part of a much bigger scientific undertaking: figuring out how we came to be the way we are.

[Image: Frank Vinken]

Earlier this year in National Geographic, I wrote about how feathers evolved long before flight. This timing naturally raises the question, how did feathered dinosaurs take to the air?  My article was accompanied by a picture from the University of Montana lab of Ken Dial, who argues that before dinosaurs flew, they flapped their wings to help them travel up and down inclines. While not all experts accept Dial’s hypothesis, it has the undeniable strength that he can gather evidence for it in living birds, rather than just inferring behavior from fossils alone.

This video shows some of the astonishing climbs birds can make with the help of some wing flapping. It’s a mix of lab climbs and footage from the wild, with an evolutionary tree of birds.

This is a skill that takes time for birds to develop, as shown in this video below. Dinosaurs might have gradually acquired the skill as well, as their arms evolved into more bird-like wings.

Dial argues that this flapping would also help on the way down, too. Here’s a young bird leaping to the ground, and flapping its wings to control its fall.

By the time dinosaurs had evolved the ability to use feathers to assist in climbs, they would have already developed the wing stroke used by birds today for true flight, as this video shows.

Even without full flight, Dial argues, flapping feathered wings would have given little feathered dinosaurs the boost they needed to escape hungry predators. And this behavior could have served as an evolutionary bridge from the land to the air.

Tip of the maniraptoran hat to Tom Holtz