Carl Zimmer's Blog, page 28

Mediocre Poison Eaters And The Imperfection of Evolution

It’s easy to forget sometimes that evolution is always a work in progress. We contemplate the eye or look upon an oak tree, and ask, how could they be any better? Somehow, in those moments of awe, we forget about detached retinas and sudden oak death. The evolutionary race is not in fact won by the perfect, but by the good-enough. And it just so happens that one of the best illustrations of evolution’s mediocrity is unfolding in front of us right now.

This episode of evolution is entirely of our own doing. In 1936, a chemical called pentachlorophenol went on the market. It was hugely popular as a way to preserve telephone poles and lumber against fungi and termites. Unfortunately, it also turned out to be toxic to humans, and once it got into the soil it could contaminate the ground for years. That’s because the molecule–five chlorine atoms decorating a ring of carbon atoms–had not previously existed in nature. Microbes had not evolved to feed on it before. It was as toxic to them as it was to us.

Starting in the 1970s,  however, scientists discovered some microbes that had begun to feed on pentachlorophenol. Pollution-eating bugs are popular in microbiology circles, because they can sometimes be deployed to clean up our messes. So a number of scientists have spent recent years dissecting the pentachlorophenol-eaters. Last year, for example, researchers published the genome of one such species, Sphingobium chlorophenolicum, which had been discovered in pentachlorophenol-laced soil in Minnesota in 1985.

When you first learn how Sphingobium eats pentachlorophenol, it inspires that same awe that eyes and oaks do. It uses a series of enzymes to pick off the chlorine atoms one at a time, like a gorilla removing spines from nettles. And yet, for all the complexity of Sphingobium‘s biochemistry, it does a pretty lousy job of feeding on pentachlorophenol.

Shelley Copley of the University of Colorado and her colleagues have tested out the individual enzymes that the bacteria use. They actually work far slower than typical enzymes involved in breaking down toxins. When they grab onto the molecule, they often lose their grip. Sometimes they grab onto an entirely different molecule instead. And while Sphingobium may be able to eat pentachlorophenol, they are not completely immune to its risks. Expose the bacteria to a high level of the pesticide, and they die.

A look at the genes that encode the enzymes reveals why they’re so mediocre: they’re new to the job. While they all act together like workers on an assembly line, they have different origins. Copley and her colleagues were able to gain some clues to those origins by comparing Sphingobium chlorophenolicum to closely related species that cannot break down pentachlorophenol. They have summed up their current understanding of the evolution of pentachlorophenol-feeding with a diagram, which I’ve reprinted below (click to enlarge). The molecules show pentachlorophenol being dismantled. The microbe’s enzymes are marked in red in each reaction arrow. (Spont. means that a reaction happens on its own–spontaneously.)

The oldest part of this pathway is marked in green. Related bacteria have PcpA and PcpE, and they use these enzymes to break down molecules that are similar to pentachlorophenol at this stage of the reactions. But the genes for the steps marked in blue and yellow were not present in that common ancestor. Instead, Sphingobium chlorophenolicum acquired them after it split off from its relatives.

Click to enlarge. Source: Genome Biol. Evol. 4(2):184–198. doi:10.1093/gbe/evr137

Horizontal gene transfer, as this process is known, is common in the microbial world. Microbes slurp up DNA from dead neighbors, viruses shuttle genes to new hosts, and sometimes microbes even build tubes to inject their genes into other microbes. Scientists became aware of horizontal gene transfer when bacteria started trading genes for antibiotic resistance, rendering wonder drugs less than wonderful. But these cases were relatively simple: a single gene could, on its own, give bacteria better protection against antibiotics.

What’s been happening in Sphingobium is more complicated. Two sets of genes have moved into the bacteria, where they have linked together, as well as to a set of genes that was already there. Together, they took on an entirely new tasks that none of them could have handled before: breaking down pentachlorophenol.

Scientists don’t yet know where those pieces of the pentachlorophenol pathway came from, or what exactly they were doing in older microbes. PcpC, the enzyme in the yellow section, is closely related to enzymes that break down proteins. In fact, PcpC can still break down proteins, although not as well as more specialized enzymes. Breaking down proteins might have been its previous job, and only later did its ability to help break down chlorine-bearing molecules come to the fore.

The genes in this pathway have been continuing to evolve over the past few decades. Natural selection favors the microbes that can grow faster on pentachlorophenol than its competitors. But that competition has not produced any gold medalists just yet. The enzymes still aren’t very well adapted to breaking down this toxic molecule.

Consider the very first step in the pathway, where PcpB picks off the first chlorine atom. Usually, enzymes make molecules less toxic than before. But PcpB does the opposite. It turns pentachlorophenol into the truly nasty tetrachlorobenzoquinone, which you do NOT want to mess with.

There are other cases in which enzymes make molecules more toxic, rather than less. But in those cases–where evolution has had more time–the enzymes are adapted to protect the cell from their toxic creation. The molecule never gets a chance to float away, free to wreak havoc, because the enzyme binds to the next enzyme, carefully handing off the prisoner.

Sphingobium can’t do that handoff. The best it can manage is to have PcpB hold onto the molecule until the next enzyme, PcpD, happens to bump into it. That strategy keeps the nasty tetrachlorobenzoquinone from escaping and killing the microbe. But it slows down the whole process of breaking down the molecule enormously.

Will the mediocre Sphingobium evolve a hand-off? Stay tuned. If it only took a few decades for the microbe to get this far, maybe we’ll witness the next step in our lifetime.

How To Evolve a Dog’s Brain (And A Human One, While We’re At It)

It’s Thursday, and that means that I’m publishing my next piece for Matter, my weekly column for the New York Times. Today, I take a look at dogs. Last month I wrote in the Times about cognitive scientists playing games with dogs to probe their behavior. But that’s just part of the story of canine research these days. There are also geneticists out there looking at the same question from a different perspective. They want to find the genes that evolved over the past 30,000 years or so to turn the brain of a wolf into the brain of a dog. The answers are now starting to emerge, and they’re fascinating. They may, in fact, tell us a lot about how we became humans. Check it out!

How To Fall In Love With Ants

Some friends and I run a website called Download the Universe, where we review ebooks about science. Here is a review that I recently published that I thought would be of interest to readers of the Loom.

Dr. Eleanor’s Book of Common Ants. Text by Eleanor Spicer Rice. Photographs by Alex Wild. Available at The School of Ants. iPad or pdf. Free.

Many plants grow a thick coat around their seeds. The coat, called an elaiosome, doesn’t do the seed any good, at least directly. Its immediate job is to attract an insect known as the winnow ant. (The photo above shows winnow ants discovering blood root seeds.) The eliaosome releases fragrant odors that lure the ants, which then carry the seed into their nest. There the ants gnaw away at the seed’s coating but spare the seed itself. The ants then carry the shucked seed back out to the forest floor, where it germinates.

The winnow ant thus act like a gardener, caring for the plants. It protects the seeds from predators that would destroy them, and it spreads them far from their parent plant. Remove winnow ants from a forest, and its populations of wildflowers will shrink.

As a resident of the northeastern United States, I always assume that all the magnificent examples of coevolution must be going on somewhere else. The jungles of Ecuador, the Mountains of the Moon–these are the places where nature-film producers go to find species exquisitely adapted to each other. This, of course, just belies my far-less-than-complete education in natural history. While reading Dr. Eleanor’s Book of Common Ants, I discovered that winnow ants are abundant here in New England, along with the rest of the eastern United States. The next time I am out on a walk in the local woods, I’m going to keep an eye out for these elegant little insects.

Dr. Eleanor’s Book of Common Ants is itself an elegant little book–and an instructive example of how ebooks can become a tool in the growing citizen science movement. “Citizen science” typically refers to research that relies not just on a handful of Ph.D. researchers, but also on a large-scale network of members of the public. Birders have been doing citizen science for over a century, and now the Internet enables people to collaborate on many other projects, from mapping neurons in the eye to folding proteins to recognizing galaxies. Many of these projects yield solid scientific results (see this paper in Nature, with over 57,000 co-authors as an example). They also provide a new way for research to draw non-scientists into their world.

At North Carolina State University, biologist Rob Dunn and his colleagues have built a little empire of citizen science projects. I myself eagerly participated in his survey of the microbial life dwelling in the human belly button. (I’ve got 58 species, which turns out to be below average.) More recently, they’ve created a project they’ve dubbed The School of Ants. Here’s how they describe it:

The School of Ants project is a citizen-scientist driven study of the ants that live in urban areas, particularly around homes and schools. Teachers, students, parents, kids, junior-scientists, senior citizens and enthusiasts of all stripes are involved in collecting ants in schoolyards and backyards using a standardized protocol so that we can make detailed maps of the wildlife that lives just outside our doorsteps. The maps that we create with these data are telling us quite a lot about native and introduced ants in cities, not just here in North Carolina, but across the United States.

The School of Ants web site has plenty of information to help amateur ant hunters recognize the species trundling across a nearby sidewalk and then share their findings. But, like most web sites, it one works best as a sprawling reference. Its architecture doesn’t lend itself well to the sustained education required to become a backyard myrmecologist. For that experience, it’s hard to beat a book.

Hence, Dr. Eleanor’s Book of Common Ants. Eleanor Spicer Rice has written a 142-page introduction to these insects. She describes 13 common American species, such as the winnow ants, and also provides a general introduction to their biology. Rice writes for a young audience, but fortunately she doesn’t see that as an opportunity to write badly. Her style is clear, fluid, and engaging. (I’m fond of the way she described winnow ants as “rusty ballerinas.”)

The design and artwork in the book are also excellent. Neil McCoy created the book using iBook Author, Apple’s free software for making ebooks for the iPad. The design is clean, despite the fact it combines text, maps, photo galleries, and videos. I still use a first-generation iPad, waiting (or hoping?) for it to die, but it never struggled as it displayed the elements of Dr. Eleanor’s Book of Common Ants. What makes it especially lovely is the abundance of photographs by Alex Wild, the Ansel Adams of arthropods. The tiny size of the photo I included with this review doesn’t do justice to his work, but the large-scale format of his images on the iPad does.

I can quibble, but not for very long. This ebook is only available for iPad, for which I blame Apple, not McCoy. (You can get a pdf version, which lacks the galleries and video.) The ebook includes Google maps for each species, but they’re not interactive. Readers are instructed to go to the School of Ants web site for interactive versions, with no link on the page to take you there. But I can’t follow this line of grousing very long before I remember that this ebook is free (thanks to the support that the project gets from sources such as the Burroughs Wellcome Fund). I would have gladly paid for it. I heartily recommended it not just to people who want to join the School of Ants project, but anyone who wants to appreciate the miniature beauty and complexity of ants. And I hope that Dr. Eleanor’s Book of Common Ants inspires other citizen science projects to produce informative ebooks of their own.

Tracing Breast Cancer’s History

Photo of Angelina Jolie by mfrissen via Creative Commons http://www.flickr.com/photos/marcof/3...

In today’s New York Times, the actress Angelina Jolie published a remarkably forthcoming op-ed about getting a double mastectomy. Jolie carries a variant of a gene called BRCA1 that makes women highly likely to develop breast and ovarian cancer. Her mother, who also carried the variant, died of ovarian cancer at age 56. Like a number of other women with her condition, Jolie decided to get a mastectomy as a preventative measure.

A number of studies have shown that bilateral risk-reducing mastectomies (the official term) do indeed reduce the risk of breast cancer in women with the BRCA1 mutation. In a study published last month in Annals of Oncology, a team of Dutch medical researchers tracked 570 women with BRCA1 (or a mutation in the related gene BRCA2). At the start of the study, all the women were healthy; 212 of them later chose to get risk-reducing mastectomies. Over the next few years, the researchers followed their progress. Sixteen percent of the women who didn’t get risk-reducing mastectomies developed breast cancer; of the women who went Jolie’s route, none did.

The initials in BRCA1 stand for breast cancer. Its name reflects how it was discovered: scientists found it as they were searching for the cause of the disease. But such names are really misnomers. After all, genes don’t simply sit in our DNA so that they can mutate in some people and make them sick. Normally, they have a job to do. In the case of BRCA1, there are many jobs. For one thing, it protects DNA from harmful mutations that can arise as it’s getting replicated. And if DNA does get damaged, the BRCA1 protein helps fix it. It joins together with several teams of other proteins, and each team carries out a different part of the complex task of DNA repair.

BRCA1, in other words, normally keeps our cells in good shape. If it mutates, though, it can’t do its jobs properly. Cells with a mutant copy of BRCA1 let mistakes slip by. Mutations in other genes can accumulate in a line of dividing cells. Some of those mutations will cause cells to die, but sometimes they have the opposite effect: the mutant cells grow and divide rapidly. As they proliferate, they accumulate even more mutations, eventually becoming full-blown cancer. As a result, women who carry BRCA mutations have a 40 to 85 percent risk of developing breast cancer during their lifetime. (They also run a 16 to 64 percent risk of ovarian cancer.)

Last year, a team of scientists at the University of Utah discovered an unexpected side effect of BRCA mutations. They looked at medical records of women who carried BRCA mutations and compared them to women with a normal version of the genes. The scientists found that women with the mutations weren’t just more likely to develop cancer. They also had more children. The effect was particularly strong among women born before 1930: they had, on average, two additional children (6.22 compared to 4.19).

The Utah scientists couldn’t say from their study how the mutations could lead to more children. But they offered one suggestion. A woman’s fertility depends on the viability of her eggs. Like other cells, eggs have caps called telomeres on the ends of their chromosomes that keep them from getting damaged. The longer the telomeres, the better shape an egg is in. Among its many jobs, BRCA1 helps control the length of telomeres. The Utah scientists suggest that mutant BRCA1 proteins may lengthen the telomeres in eggs, keeping them more viable.

BRCA mutations are so good for fertility that Jack da Silva, a biologist at the University of Adelaide,  has pointed out that they should be a lot more common. Only a few percent of women carry them, but they enable women to have so many more children, you’d expect the mutation to become more common with each generation. Within a few centuries of the mutation first appearing, everyone should have it.

Da Silva proposes that the mutations hang in an evolutionary balance. Before the age of 40, a woman with a BRCA mutation only has a 20% chance of developing breast cancer. That risk rises to 37 percent by the age of 50 and continues going up; by the age of 70, it’s 70 percent. In other words, these women have good odds of surviving to the point at which they can give birth to children, but they’re less likely to be alive to see their own children become parents.

A number of biologists have argued that grandmothers have played an important part in the survival of their grandchildren. In fact, some maintain that their help is so valuable that menopause evolved as a result. Women who stop raising their own children can better channel their efforts into helping to raise their grandchildren. Women with BRCA mutations are less likely to be able to provide that help. As a result, Da Silva suggests, the odds of their grandchildren surviving may have been somewhat lower than for grandmothers without the mutations.

This balance could account for the puzzling nature of BRCA mutations. They’re more common than other potentially fatal disorders like cystic fibrosis, and they’re unable to spread to more than a few percent of the population. It is this ancient legacy of BRCA’s many effects that women like Jolie are grappling with today.

[Update 5/14: I corrected the cause of Angelina Jolie's mother's death from breast to ovarian cancer.]

The Lurker: How A Virus Hid In Our Genome For Six Million Years

In the mid-2000s, David Markovitz, a scientist at the University of Michigan, and his colleagues took a look at the blood of people infected with HIV. Human immunodeficiency viruses kill their hosts by exhausting the immune system, allowing all sorts of pathogens to sweep into their host’s body. So it wasn’t a huge surprise for Markovitz and his colleagues to find other viruses in the blood of the HIV patients. What was surprising was where those other viruses had come from: from within the patients’ own DNA.

HIV belongs to a class of viruses called retroviruses. They all share three genes in common. One, called gag, gives rise to the inner shell where the virus’s genes are stored. Another, called env, makes knobs on the outer surface of the virus, that allow it to latch onto cells and invade them. And a third, called pol, makes an enzyme that inserts the virus’s genes into its host cell’s DNA.

It turns out that the human genome contains segments of DNA that match pol, env, and gag. Lots of them. Scientists have identified 100,000 pieces of retrovirus DNA in our genes, making up eight percent of the human genome. That’s a huge portion of our DNA when you consider that protein coding genes make up just over one percent of the genome.

Scientists have studied these so-called endogenous retroviruses both in humans and in other species, and the evidence all points to the same scenario for how they genetically merged with us. Our ancestors were infected with retroviruses on a regular basis. On rare occasion, a virus infected a sperm or egg and managed to end up in an embryo. Every new cell in the embryo inherited the retrovirus DNA implanted in its genome. And then the embryo grew up into an adult, which then had offspring of its own, and passed the virus DNA on as well.

At first, the virus still retained some of its old powers. Its DNA could sometimes still give rise to new viruses. Mutations arose in the viral genes, and they might prevent it from making shells. Yet the dying virus could still make a new copy of its genes and insert them back into its host genome. That would explain why it’s possible to classify our many endogenous retroviruses into different families. The families are made up of new copies of an ancestral virus.

Eventually, however, the endogenous retroviruses got so hobbled by mutations that they became nothing more than baggage. (In some cases, we’ve domesticated their genes, co-opting them for our own functions, such as building a placenta.) Given that many matching endogenous retroviruses can be found in other primates, this process has been going on for millions of years–even tens of millions.

The world of our inner viruses is still a murky, mysterious one that scientists are still surveying. And Markovitz’s discovery enabled him to add considerably to our understanding of these shadowy creatures. He discovered new members of a particularly interesting class of endogenous retroviruses–ones that, even today, can still have life breathed into them.

Markovitz and his colleagues analyzed the sequence of the virus genes they found in the patients with HIV. The genes belonged to a family of endogenous retroviruses called HERV-K, but they were not quite like any known HERV-K virus previously found.

The Michigan scientists wondered if this new HERV-K virus was hidden in the human genome. They checked the most complete draft of the human genome and couldn’t find a match. They knew that the human genome sequence was only about 95% finished, so they turned instead to the chimpanzee genome, on the off chance that the virus had infected the common ancestor of humans and chimpanzees over six million years ago. Bingo: a single copy of the virus turned up in the chimp genome. They dubbed it K111.

Having found this match, the scientists decided to return to the human genome and search for K111. They isolated DNA from their HIV patients, as well as from healthy people. They then split apart the two strands of the DNA and added a short piece of DNA that would bind to K111, should it be lurking there. In all 189 of their subjects, the scientists found the virus’s DNA.

Remarkably, though, the scientists didn’t find just one copy of K111 in each of their subject’s genomes, as is the case in chimps. The more the scientists looked, the more variants they found. Some K111 viruses were fairly intact, while others were vestiges. The scientists found over 100 copies of the virus in the human genome, scattered across fifteen chromosomes.



To figure out the origin of K111, the scientists looked back at other primates. They couldn’t find a version of K111 in any species other than chimpanzees. They concluded that the virus infected our ancestors not long before the split between humans and chimpanzees roughly six million years ago.

To find out what happened next, Markovitz and his colleagues turned to the genomes of extinct humans. Svante Paabo of the Max Planck Institute and his colleagues have sequenced the Neanderthal genome, as well as the genome of a lineage of mysterious cousins of Neanderthals, known as Denisovans. Our own ancestors diverged from those of Neanderthals and Denisovans about 800,000 years ago. Markovitz and his colleagues looked for K111 in their genomes, and there it was. The scientists found seven copies of K11 in Neanderthal DNA and four in the Denisovan genome.

This finding suggests that between 6 million and 800,000 years ago, K111 was duplicated a few times at a fairly slow pace. It’s possible that Markowitz and his colleagues missed some other copies because the reconstruction of those ancient genomes wasn’t quite accurate enough for their search. But even if we generously assumed that Neanderthals and Denisovans had twenty K111 viruses apiece, that’s still a small fraction of the 100 or more copies of K111 the scientists found in the human genome. It was only later, in the past 800,000 years, that K111 started proliferating at a faster pace.

One reason that K111 has gone overlooked till now is that it found a good place to hide–the center of chromosomes. This region, called the centromere, is a genomic Bermuda Triangle. It’s loaded with lots of short, repetitive stretches of DNA. When scientists reconstruct the sequence of a genome, they break DNA down into many overlapping segments, which they then try to rebuild based on overlapping similarities. Centromere DNA is so similar to itself that it’s easy to line up fragments in many different arrangements. As a result, centromeres make up much of the last 5% of the human genome that has yet to be mapped.

Another reason K111 has been able to hide for so long is that it’s fairly feeble. It lacks genes to make shells, so it can’t escape from its host cells any more. In fact, it was our own centromeres that appear to have made all the extra copies of K111. The repeating DNA in centromeres is not just tricky for human gene sequencers. It’s also tricky for the enzymes in a cell that make new copies of our DNA. They can slip up and accidentally swap segments from two chromosomes. K111 was thus able to spread from the centromere of one chromosome to another. Our cells also stutter sometimes when they try to copy centromere DNA, making extra copies of segments there. Markovitz and his colleagues argue that this is how new copies of K111 proliferated within each centromere.

Ironically, it was the HIV in the patients Markovitz and his colleagues studied which brought K111 back to light. When people get infected with HIV, the virus makes a protein called Tat which uncoils tightly wound stretches of human DNA, which allows its host cell to make more HIV at a faster rate.

Markovitz and his colleagues wondered if the Tat in their HIV-infected patients was spurring cells to also make copies of K111. To find out, they injected Tat proteins into human cells that were free of HIV. As they predicted, out came new genes for K111.

It’s conceivable that K111 interacts with HIV to contribute to AIDS, but Markovitz and his colleagues found no evidence of that. It’s certainly worth investigating further. But there’s another reason to keep learning about K111.  Now that scientists have discovered K111, they can look for more copies of it in centromeres. Markovits suggests that their distinctive genes might serve as a kind of genetic barcode that could help genome mappers orient themselves in the hall of mirrors that is centromere DNA. Perhaps the human genome sequence will finally be completely mapped thanks to a virus that has been hiding in it for six million years.

(For more information, see my book, A Planet of Viruses.)

Cicadas: The Methuselah Horde (And News About A New Column!)

Periodical cicada. Photo by Alex Wild. http://bit.ly/11VYduY

I’ve been writing about science for the New York Times for over eight years now, but today I’m starting something new there. I’ll be writing a column (called “Matter”) every week. The first column is just out. I take a look at the cicada invasion we’re facing here in the eastern United States, and step back to consider the fact that these creatures have the longest lifespan of any insect–seventeen years, almost all of which they spend underground. It’s a bizarre life cycle that’s been millions of years in the making.

My columns will appear each Thursday on the Science Times page online, and some will also appear the following Tuesday in the print edition ofthe  Science Times. Check it out! And do NOT miss Jonathan Corum’s fascinating timeline graphic of the past century of cicada broods.

How Our Outside World Turned Inward

The nervous system that sprouts from the brain may seem like an incomprehensible tangle. But anatomists can divide it pretty cleanly into two parts. One part is directed to the outside world, while the other is turned inward.

The somatic nerves take in sensory information from the outside world from our eyes, nose, ears, and skin. They also relay commands to move muscles. They are essential for our responding to the external world. Visceral nerves, on the other hand, detect information about our internal state. They sense blood pressure, the queasiness in our guts, even the level of oxygen in our bodies. And they also send signals to those organs, causing racing hearts, gasping lungs, and puking stomachs.

Recently, Marc Nomaksteinsky of Institut de Biologie de l’École Normale Supérieure in Paris and his colleagues explored the evolution of this divide. They discovered evidence suggesting that it’s a profoundly ancient one.

Tracking the evolution our nervous system is especially hard. Teeth and bones leave behind sturdy fossils that contain clues to how earlier forms gave rise to later ones–a fish’s fin becoming a foot, for example. Neurons dissolve away after death. The brain, with the consistency of custard, cannot withstand the elements and leaves behind a hollow cavity. That cavity can tell scientists about the size and shape of a brain, but not much about the function of the brain within. The holes through which neurons pass through the skull and other bones offer the skimpiest of hints about what signals they relayed in life.

Scientists can add to those skimpy hints from fossils by comparing living animals. Humans and other living primates share certain features in their brains not found in other animals. The emergence of our primate ancestors 60 million years ago was marked by a massive expansion of the visual cortex, for example.

Nomaksteinsky and his colleagues used a different method to explore the evolution of our two nervous systems. The somatic and visceral nerves in our bodies have distinctive molecular profiles. Each type makes its own combination of proteins to carry out its own particular task. Almost all the visceral nerves, for example, make a protein called Phox2b. The somatic nerves that relay sensory information, on the other hand, all make a protein called Brn3.

The scientists wondered if they could find neurons with these molecular profiles in distantly related animals. They chose to look at a snail and a related species called Aplysia. Both species are mollusks, which sit on a branch of the animal evolutionary tree far from our own. The common ancestor of mollusks and us lived about 600 million years ago, at an early stage in animal evolution.

Nomaksteinsky and his colleagues found versions of Phox2b, Brn3, and other markers of somatic and visceral nerves in the mollusks. What’s more, they found the two kinds of markers in two distinct sets of neurons. This is pretty remarkable when you consider how different our nervous systems are. We humans and other vertebrates have one big brain in our head, out of which sprouts a system of neurons. Molluscs have a cluster of neurons in their head, but they also have clusters in other parts of their body, all connected in what looks like a complex snarl.

But when you consider what the two kinds of neurons do in mollusks, some similarities emerge. Some of mollusk neurons with a “somatic” profile are sensitive to touch and pain–just like some of our own somatic neurons are. Some of mollusk neurons with a “visceral” profile control a siphon they use to suck in water in order to filter food. That’s the sort of function our own visceral nerves carry out with our lungs and digestive system.

These results suggest that a snail’s nervous system is split between the outer and inner worlds much like ours is. The molecular profile of their neurons suggests the split didn’t evolve indepedently, once in molluscs and vertebrates. It arose instead in our common ancestor–a small, worm-shaped creature crawling on the ocean floor.

In a commentary on the paper, Paola Bertucci and Detlev Arendt of European Molecular Biology Laboratory speculate on how these two parts of the nervous system may have arisen. In us, the visceral system senses the inner chemistry of our bodies. But for an ocean worm 600 million years ago, this kind of information was important to sense in its external environment, too–the pH of the sea water, its saltiness, its oxygen levels, and so on. Perhaps the entire nervous system started pointing outward. Only later did it evolve to tell us something about our inner world.

Charlemagne’s DNA and Our Universal Royalty

Nobody in my past was hugely famous, at least that I know of. I vaguely recall that an ancestor of mine who shipped over on the Mayflower distinguished himself by falling out of the ship and having to get fished out of the water. He might be notable, I guess, but hardly famous. It is much more fun to think that I am a bloodline descendant of Charlemagne. And in 1999, Joseph Chang gave me permission to think that way.

Chang was not a genealogist who had decided to make me his personal project. Instead, he is a statistician at Yale who likes to think of genealogy as a mathematical problem. When you draw your genealogy, you make two lines from yourself back to each of your parents. Then you have to draw two lines for each of them, back to your four grandparents. And then eight great-grandparents, sixteen great-great-grandparents, and so on. But not so on for very long. If you go back to the time of Charlemagne, forty generations or so, you should get to a generation of a trillion ancestors. That’s about two thousand times more people than existed on Earth when Charlemagne was alive.

The only way out of this paradox is to assume that our ancestors are not independent of one another. That is, if you trace their ancestry back, you loop back to a common ancestor. We’re not talking about first-cousin stuff here–more like twentieth-cousin. This means that instead of drawing a tree that fans out exponentially, we need to draw a web-like tapestry.

In a paper he published in 1999 [pdf], Chang analyzed this tapestry mathematically. If you look at the ancestry of a living population of people, he concluded, you’ll eventually find a common ancestor of all of them. That’s not to say that a single mythical woman somehow produced every European by magically laying a clutch of eggs. All this means is that as you move back through time, sooner or later some of the lines in the genealogy will cross, meeting at a single person.

As you go back further in time, more of those lines cross as you encounter more common ancestors of the living population. And then something really interesting happens. There comes a point at which, Chang wrote, “all individuals who have any descendants among the present-day individuals are actually ancestors of all present-day individuals.”

In 2002, the journalist Steven Olson wrote an article in the Atlantic about Chang’s work. To put some empirical meat on the abstract bones of Chang’s research, Olson considered a group of real people–living Europeans.

The most recent common ancestor of every European today (except for recent immigrants to the Continent) was someone who lived in Europe in the surprisingly recent past—only about 600 years ago. In other words, all Europeans alive today have among their ancestors the same man or woman who lived around 1400. Before that date, according to Chang’s model, the number of ancestors common to all Europeans today increased, until, about a thousand years ago, a peculiar situation prevailed: 20 percent of the adult Europeans alive in 1000 would turn out to be the ancestors of no one living today (that is, they had no children or all their descendants eventually died childless); each of the remaining 80 percent would turn out to be a direct ancestor of every European living today.

Suddenly, my pedigree looked classier: I am a descendant of Charlemagne. Of course, so is every other European. By the way, I’m also a descendant of Nefertiti. And so are you, and everyone else on Earth today. Chang figured that out by expanding his model from living Europeans to living humans, and getting an estimate of 3400 years instead of a thousand for the all-ancestor generation.

Things have changed a lot in the fourteen years since Chang published his first paper on ancestry. Scientists have amassed huge databases of genetic information about people all over the world. These may not be the same thing as a complete genealogy of the human race, but geneticists can still use them to tackle some of the same questions that intrigued Chang.

Peter Ralph and Graham Coop, two biologists at the University of California, Davis, decided to look at the ancestry of Europe. They took advantage of a compilation of information about 2257 people from across the continent. Scientists had examined half a million sites in each person’s DNA, creating a distinctive list of genetic markers for each of them.

You can use this kind of genetic information to make some genealogical inferences, but you have to know what you’re dealing with. Your DNA is not a carbon copy of your parents’. Each time they made eggs or sperm, they shuffled the two copies of each of their chromosomes and put one in the cell. Just as a new deck gets more scrambled the more times you shuffle it, chromosomes get more shuffled from one generation to the next.

This means that if you compare two people’s DNA, you will find some chunks that are identical in sequence. The more closely related people are, the bigger the chunks you’ll find. This diagram shows how two first cousins share a piece of DNA that’s identical by descent (IBD for short).

Source: http://gcbias.org/european-genealogy-...

Ralph and Coop identified 1.9 million of these long shared segments of DNA shared by at least two people in their study. They then used the length of each segment to estimate how long ago it arose from a common ancestor of the living Europeans.

Their results, published today in PLOS Biology, both confirm Chang’s mathematical approach and enrich it. Even within the past thousand years, Ralph and Coop found, people on opposite sides of the continent share a lot of segments in common–so many, in fact, that it’s statistically impossible for them to have gotten them all from a single ancestor. Instead, someone in Turkey and someone in England have to share a lot of ancestors. In fact, as Chang suspected, the only way to explain the DNA is to conclude that everyone who lived a thousand years ago who has any descendants today is an ancestor of every European. Charlemagne for everyone!

If you compare two people in Turkey, you’ll find bigger shared segments of DNA, which isn’t surprising. Since they live in the same country, chances are they have more recent ancestors, and more of them. But there is a rich, intriguing pattern to the number of shared segments among Europeans. People across Eastern Europe, for example, have a larger set of shared segments than people from within single countries in Western Europe. That difference may be the signature of a big expansion of the Slavs.

Ralph and Coop’s study may provide a new tool for reconstructing the history of humans on every continent, not just Europe. It will also probably keep people puzzling over the complexities of genealogy. If Europeans today share the same ancestors a thousand years ago, for example, why don’t they all look the same?

Fortunately, Ralph and Coop have written up a helpful FAQ for their paper, which you can find here.

[Update: Adjusted the estimated generations since Charlemagne to thirty.]

Venomous TV

Here’s a gruesome treat. NOVA just did a show on venom, and you can watch it online.

Ed Yong and I have written to unhealthy lengths about the evolution of venom, so if you prefer venom in text to venom in video–or if you just want some background–check these posts out.

Pythons are still a little venomous

On the Origin of Venom

Painkilling chemicals with no side effects found in black mamba venom

World’s 2nd deadliest poison, in an aquarium store near you

How a pit viper saved millions of lives: Snakes as drug factories

Venomous shrews and lizards evolved toxic proteins in the same way

Feathers: 200 Million Years In Just Over 3 Minutes

Last year I wrote in National Geographic about the long, remarkable history of feathers. The folks at TED-Ed (the educational wing of TED) invited me to boil down that history to about three minutes–accompanied by a splendid animation by Armeilia Leung. Here’s what we came up with.

For more information, you can visit the video’s page at TED-Ed.