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. Read 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.
If you’re a regular reader of the Loom, you’re no doubt familiar with the parasite Toxoplasma gondii. If you’re not, now is the perfect time to meet this sinister creature which may very well be residing in your brain. It seems like every year or two, it gets more remarkable, and today it’s taken another step into awesomeness.
Here’s a quick Toxoplasma primer. It’s a single-celled protozoan that reproduces inside the digestive tract of cats. The cats poop out egg-like Toxoplasma cells into kitty litter and dirt. Other animals take up the parasite, which makes its way into their tissues, especially the brain. There it forms cysts that can linger for years or decades. Only if that animal gets eaten by a cat can Toxoplasma complete its life cycle.
This life cycle opens up opportunities for Toxoplasma to evolve. For example, natural selection should favor mildness in the parasite in its hosts, because cats do not like to eat corpses. And, indeed, Toxoplasma is fairly harmless, only causing trouble to people with suppressed immune systems. (Hence the rule that pregnant women should not handle kitty litter. If they get infected by Toxoplasma for the first time, the parasite runs amok in the fetus.) On the other hand, if there’s any way for the parasite to increase the odds that it can get from prey to cat, natural selection may favor genes for that strategy too.
And it turns out that Toxoplasma does have that very ability. In studies on rats, scientists have found that infected rodents lose their fear of the scent of cats. In fact–and please remember, I am a science writer, not a Hollywood script doctor–the rats may even become sexually aroused by the smell of cats. They embrace their doom, and the parasite benefits.
These findings have lots of interesting implications for humans, because perhaps a quarter of all people on Earth carry these parasites in their heads, where they no doubt secrete their mind-altering compounds. There’s some preliminary work that suggests some changes to the personality of infected people, but nothing definitive.
That would be enough for Toxoplasma to earn its place in the Parasite Hall of Fame. But, no, it needed to go one better.
It turns out that rats and other non-cat hosts can spread Toxoplasma to each other through sex. The first reports have only just emerged from studies on dogs and sheep. Recently Ajai Vyas, a neuroscientst at Nanyang Technological University in Singapore, decided to see whether rats can spread Toxoplasma the same way. In the journal PLoS One, he and his colleagues describe how they mated infected males with uninfected females. They found Toxoplasma in the male rats’ semen, and, after mating, in the female rats’ vaginas. And later, they found signs of Toxoplasma in the female rat brains.
These are Toxoplasma cysts moving from rat to rat, so this exchange is kind of like a side track on the parasite’s life cycle. But it still benefits Toxoplasma, because it means it can infect even more potential prey that may get eaten by cats. And so the logic applies once more: if Toxoplasma can raise the odds of getting from infected males to uninfected females, it may have more reproductive success.
You know where this is going–it’s turning into a David Cronenberg horror movie with an all-rodent cast. Vyas wondered if there’s any difference in how female rats mate with infected and uninfected males. So he and his colleagues put a male rat with Toxoplasma at one end of a two-armed maze, and an uninfected male in the other arm. Females then got to choose which rat to approach. Vyans found that they preferred the infected males, spending more time with them and mating more often.
In other words, Toxoplasma makes its host sexy, in order to get into other hosts through sex.
As I wrote in Parasite Rex, many parasites have evolved the ability to manipulate hosts. But I was disappointed to find no good examples of parasites that manipulate the sexual behavior of their hosts. In fact, female rats have actually evolved to steer clear of male rats infected with some other parasites. They can detect these infections even when the male rats look healthy, and they avoid these males to avoid getting sick. Now Vyas’s research suggests that there is at least one parasite that manipulates sex. Toxoplasma may be exquisitely unusual among parasites. But it’s also possible that there are other sex-hijacking creatures lurking out there. As for what this means for humans, I should point out there’s zero evidence of it moving from person to person, nor is there any evidence of it affecting the sexual behavior of humans. Then again, nobody has looked. For now, you can just let your inner Cronenberg take matters from here….
There are many weird viruses on this planet, but none weirder–in a fundamentally important way–than a group known as the giant viruses.
For years, they were hiding in plain sight. They were so big–about a hundred times bigger than typical viruses–that scientists mistook them for bacteria. But a close look revealed that they infected amoebae and built new copies of themselves, as all viruses do. And yet, as I point out in A Planet of Viruses, giant viruses certainly straddle the boundary between viruses and cellular life. Flu viruses may only have ten genes, but giant viruses may have 1,000 or more. When giant viruses invade a host cell, they don’t burst open like other viruses, so that their genes and proteins can disperse to do their different jobs. Instead, they assemble into a “virus factory” that sucks in building blocks and spits out large pieces of future giant viruses. Giant viruses even get infected with their own viruses. People often ask me if I think viruses are alive. If giant viruses aren’t alive, they sure are close.
Ever since giant viruses were first unveiled seven years ago, scientists have argued about the origins of these not-so-wee beasties. Many of their genes are different from those found in cellular life forms, or even other viruses. It’s possible that giant viruses amassed their enormous genetic armamentarium over billions of years, picking up genes from long-extinct host or swapping them with other viruses we have yet to find. Other scientists have suggested that giant viruses started out giant–or even bigger than they are today. Some have even argued that they represent a new domain of life, although others aren’t so sure.
A new study suggests that giant viruses are indeed ancient. It is the work of a team of French researchers led by Jean-Michel Claverie, who went searching for new giant viruses in the waters near a marine biology station in Chile. They found a new kind so different from other giant viruses that they gave it a name of its own:
It’s astonishing to me that such a glorious name wasn’t already taken. In the dinosaur world, people are always hunting for Latin ways to say, “I’ve got a really big dinosaur.” Supersaurus, Ultrasaurus, Megalosaurus, Truckasaurus. The name Megavirus is truth in advertising. Its genome is 1.259 million base pairs long, which is 6.5 percent longer than the previous record holder among giant viruses. In that abundance of DNA are 1120 genes. That’s hundreds more genes than found in a lot of bacteria. (You can browse its genome for yourself here.)
Claverie and his colleagues compared the genes in Megavirus to the best-studied of the giant viruses, Mimivirus. They could not find matches for 258 Megavirus genes in Mimivirus. But they found counterparts to most of its genes, including genes for distinctively giant-virus features such as the viral factory. (The inset in the picture above shows the portal of a Megavirus viral factory, called a “stargate.” It’s similar to the stargate found in Mimivirus.) Mimiviruses have some genes for building and folding proteins, and so do Megavirus.
These results lead Claverie and his colleagues to conclude that giant viruses started out giant. They might have even been some full-blown cellular life form. In the Mimivirus and Megavirus lineage, the genes mutated in different trajectories, and new copies of genes arose, producing different gene families. The lack of 258 Megavirus genes in Mimivirus might not mean that Megavirus picked up those genes from other sources. It’s possible that Mimivirus lost those genes. Likewise, Megavirus may have lost hundreds of genes as well. Giant viruses might thus be relicts of the first chapters of the history of life. (You can read more about this scenario in this 2010 review by Claverie: pdf.)
Fortunately, there’s a straightforward way to test this hypothesis: find more giant viruses and see if they fit the pattern. Giant viruses seem to thrive in all sorts of habitats, so there should be no end of new species to find. And given that it didn’t take long to trump the old genome-size record with Megavirus, you can expect scientists to find even bigger viruses somewhere on Earth.
Whether they should call these new species Truckavirus, I leave to greater minds.
Reference: “Distant Mimivirus relative with a larger genome highlights the fundamental features of Megaviridae” Defne Arslan, Matthieu Legendre, Virginie Seltzer, Chantal Abergel, and Jean-Michel Claverie. PNAS, in press. Link [should work by the end of this week]
Once more we are going through the annual ritual of the Nobel Prize announcements. The early morning phone calls, the expressions of shock, the gnashing of teeth in the betting pools. In the midst of the hoopla, I got an annoyed email on Tuesday from an acquaintance of mine, an immunology grad student named Kevin Bonham. Bonham thought there was something wrong with this year’s Prize for Medicine or Physiology. It should have gone to someone else.
Kevin lays out the story in a new post on his blog, We Beasties. The prize, he writes, “was given to a scientist that many feel is undeserving of the honor, while at the same time sullying the legacy of my scientific great-grandfather.” Read the rest of the post to see why he feels this way.
Kevin emailed me while he was writing up the blog post. He wondered if I would be interested in writing about this controversy myself, to give it more prominence. I passed. Even if I weren’t trying to carry several deadlines on my head at once, I would still pass. As I explained to Kevin, I tend to steer clear of Nobel controversies, because I think the prize is, by definition, a lousy way to recognize important science. All the rules about having to be alive to win it, about how there can be no more than three winners–along with the lack of prizes for huge swaths of important scientific disciplines–make these kinds of disputes both inevitable and tedious.
The people behind the Nobel Prize, I should point out, have done a lot of good. Their web site is a fine repository of information about the history of science. I’ve tapped it many times while working on books and articles. There’s also something pleasing to see the world drawn, for a couple days at least, to the underappreciated byways of science. If the Nobel Prize makes more people aware of quasicrystals, the Prize is doing something unquestionably wonderful.
But the vehicle that delivers this good is fundamentally absurd. The Nobel Prize rules say no more than three people can win an award, for example. This year’s prize for physics went to Saul Perlmutter, Brian Schmidt, and Adam Riess for their work on the
dark energy that is accelerating the accelerating expansion of the universe. Half went to Perlmutter, and a quarter went to Riess and Schmidt. But, of course, scientists do not work in troikas. It wouldn’t even make sense to say that three people could accept the prize on behalf of three labs. Science is a stupendously complex social undertaking, in which scientists typically become part of shifting networks over the course of many years. And those networks are not just made up of happy friends collaborating on projects together. Rivals racing for the same goal can actually speed the pace towards discovery.
Now, some individual scientists are certainly remarkable people. But the Nobel Prize doesn’t merely recognize them for being remarkable individuals. The citations link each person to a discovery, as if there was some sort of equivalence between the two. But discoveries are usually a lot bigger than one person, or even three.
In his wonderful book The 4% Percent Universe, Richard Panek describes the history of the research that led to this year’s physics prize. I read the book to review it for the Washington Post, and I was particularly taken by a story at the end. In 2007, the Gruber Prize, the highest prize for cosmology research, was awarded for the research. Schmidt haggled with the prize committee until they agreed to widen the prize to all 51 scientists who had been involved in the two rival teams. Thirty-five of them traveled to Cambridge for the ceremony. It would have been fun to watch Schmidt go up against the Nobel Prize committee. He would have lost, of course, but at least he would have made an important point.
Should scientists get credit for great work? Of course. But that’s what history is for. Charles Darwin and Leonardo da Vinci never got the Nobel Prize, but somehow we still manage to remember them as important figures anyway. The time that’s spend arguing over whether someone should get fifty percent of a prize or twenty-five percent or zero percent could be spent on much better things, like more science.
[Update: Revised post to clarify that the prize was for research on the acceleration of the universe, not the dark energy many think is driving the acceleration.]
The man is Lee Berger, a paleoanthropologist at the University of Witwatersrand in South Africa. He’s holding the skull of Australopithecus sediba, a 1.98 million year old relative of humans, otherwise known as a hominin. In April 2010 Berger and his colleagues first unveiled the fossil in the journal Science. As I wrote in Slate, Berger argued that A. sediba was the closest known cousin to our genus Homo. Hominins branched off from other apes about 7 million years ago, but aside from becoming bipedal, they were remarkably like other apes for about five million years. Among other things, they were short, had long arms, and had small brains. Berger and his colleagues saw in A. sediba what biologists often find in transitional forms–a mix of ancestral and newer traits. It has Homo-like hands, a projecting nose, and relatively long legs. It was intermediate in heigh between earlier hominins and the tall Homo. And it still had a small brain and long arms. (In August, Josh Fishman wrote a feature for National Geographic on A. sediba, complete with excellent reconstructions.)
It wasn’t just finding such a potentially significant fossil that would make you smile if you were Lee Berger. It’s how much stuff he and his colleagues have found. The skull that Berger holds would be enough to keep several scientists busy for years. But Berger and his team have much more. In fact, A. sediba is, in some ways, now even better represented than far more recent hominin relatives.
Today, Science has turned over much of this week’s issue to follow-up papers from Berger’s team, in which they share some of the goodies. Here, for example, is A. sediba’s hand. Before this specimen came to light, paleoanthropologists had much less to look at to study the origin of the human hand. The best specimen came from a 1.75 million year old hominin called Homo habilis. It got the name Homo in part because the fossils were found along with stone tools, which were considered a sign of a very human-like creature. Researchers also found bones from its hand–but only 13 fragments. In this picture of A. sediba‘s hand, just about every bone is real. This is what paleoanthropologists dream about at night.
Tracy Kivel, a paleoanthropologist at the Max Planck Institute, led a team of researchers who compared A. sediba’s hand to the hands of humans, chimps, gorillas, and extinct hominins. They found even more mingling of old and new traits than before. The hand has ridges for powerful muscles that run up the length of the hand. Chimpanzees have muscles like these, which give them stronger grips as they climb around in trees. Earlier hominins have them too. We don’t. Instead, we have long thumbs and fleshy pads on our finger tips, which are great if you’ve come to depend on your skill to make and use tools. A. sediba has them too.
Scientists have found likely hominin stone tools dating back 2.6 million years ago; last year a team of researchers kicked up some controversy by claiming to have found signs of stone tools 3.4 million years ago. It’s clear that by the time A. sediba came on the scene, hominins had been using stone tools for hundreds of thousands of years. It’s too bad that Berger and his colleagues haven’t found any tools alongside A. sediba’s bones, to see what they could do with these transitional hands. Then again, why should he get all the fun?
Things got particularly intriguing when Kivel and company compared A. sediba‘s hand to Homo habilis’s. Remember, Homo habilis is about 250,000 years younger than A. sediba. Yet A. sediba‘s hand is actually more like our own than that of Homo habilis. It’s got some wrist bones that are shaped to handle strong forces transmitted from the thumb–the sort of forces you might expect from whacking stones together to make a cleaver, for example. Evidence such as this suggests that Homo habilis branched off first from the ancestors of A. sediba and later hominins like ourselves, and then later A. sediba branched off from our own lineage. Along the way, the hand gradually became less adapted for tree-climbing, and acquired more traits we use to handle tools.
In other papers, scientists take a look at A. sediba‘s brain and hips. The two are more intimately associated than you might think at first. We have huge brains even at birth, which make child-bearing a tricky proposition in our species, because they have to be able to pass through the birth canal. We humans have wide hips compared to other apes, and some researchers have argued that they evolved in tandom with our expanding brains. (See this column I wrote recently for more compensations in our bodies for big brains.) But it turns out that A. sediba–which had a small brain–already had broader hips than earlier hominins. Whatever drove its hip expansion, a big head wasn’t it.
While the A. sediba brain was small, it demonstrates that in hominin brain evolution, size isn’t everything. The skull Berger holds here contains a beautifully preserved cavity inside. When he and his colleagues put the fossil in a scanner, they were able to reconstruct the shapes of a lot of the left hemisphere of the brain and the front chunk of its right. The shapes of some parts of the brain (in particular, a part of the brain called orbitofrontal cortex) are more like our own than like earlier hominins.
Reading this, I can’t help but dabble in a little paleo-phrenology. The orbitofrontal cortex is a crucial node in our emotional network, where neurons assign value to things and can tamp down or ramp up our automatic responses of fear and delight. Did a glimpse of human feelings mark this great transition, long before human-sized brains evolved?
I doubt scientists will ever answer that question, but not to worry: there are many more answers A. sediba will be able to provide.
[Images: Berger, courtesy of Lee Berger and University of Witwatersrand; hand and pelvis by Peter Schmid, courtesy of Lee Berger and University of Witwatersand; brain, photo by ESRF/KJ Carlson, courtesy of Lee Berger and the University of Witwatersrand]
In 1833, John Obadiah Westwood, a British entomologist, tried to guess how many species of insects there are on Earth. He extrapolated from England to Earth as a whole. “If we say 400,000, we shall, perhaps, not be very wide of the truth,” he wrote. Today, scientists have found over a million species of insects and keep finding more every year.
The question of how many species there are on Earth has been a tricky one ever since Westwood’s day. I’ve written a story for the New York Times about a new estimate that was published today: 8.7 million.
What makes the paper particularly interesting is that it introduces a new method for estimating biodiversity. The method is based on Linnean taxonomy. While we have lots of new species left to find, we may have found most of the classes, orders, and phyla. It turns out that for a number of groups–mammals, birds, and so on–the numbers of each of these rankings rise as you descend the hierarchy.
Here’s a diagram that summarizes this striking pattern (courtesy of the Census of Marine Life). I couldn’t fit it into the story, so I thought I’d show it here:
The scientists reasoned that we’re probably closer to having found most kingdoms, classes, and other high level groups. So they used this relationship to estimate how many species there are in well-studied groups like mammals and birds. They found this method got them a number close to the actual number of species. So they applied to other groups, such as plants and fungi.
As I write in the article, some experts love this method, and some don’t think much of it. I couldn’t get into deep details in a 1,000 word piece. Here’s part of a long email I got from Lucas Joppa, an ecologist at Microsoft Research in Cambridge, England. Joppa thinks the new method is important and intriguing. And he added some interesting thoughts about why knowing this number matters–aside from just being a very basic question that’s worth answering because we can–
I do think that it matters that we try to estimate this number, although given that we are talking about millions, I don’t really think it changes our daily perception of how many species there are (the human mind has problems with any number larger than a few hundred!). Moreover, I’m not quite so sure it matters if we are able to put an exact figure of how many species there really are, as when you look at the scope of the problem (2 million currently described, likely 7 million more!) it is unlikely that we will ever reach a full census of life on earth.
That said, the goal of coming up with a sensible estimate is not only noble, but worthy from a conservation perspective…the species currently unknown to science (at least in a terrestrial sense for well-known groups such as flowering plants) are likely to have ecological traits that are correlated with extinction risk (small ranges, rare within those ranges, etc.). Because of this, putting a number on the total number of species gives us insight into the number of missing species, and thus insight into the increase in the estimated numbers of species threatened with extinction around the world. In a recent paper in the Proceedings of the National Academy of Sciences, Stuart Pimm and I, along with collaborators, show that at least for one taxonomically important group (flowering plants), those species currently “missing” (ie, undiscovered) are most likely to be found in places that are already identified as global conservation priorities.
So, the good news is that even without having a full catalogue of life, the global conservation community is already actively engaged in protecting those places where species are most at risk (ie, Biodiversity Hotspots, locations with high number of species found nowhere else, but with extensive (>70%) of natural habitat loss). The bad news is that most new species will come from places around the world most at risk! As you can see from that direct example, while knowing every single species on earth is not a likely scenario, estimating information about those species, as Mora et al. do, can drastically change the way we view current estimates of species extinction risk around the world.
In the wake of last year’s earthquake in Haiti, cholera arrived on the island for the first time in 60 years. According to the World Health Organization, 419, 511 Haitians got sick with cholera as of July 31, of which 5,968 died. The infection rate is dropping right now, but the arrival of Hurricane Irene could change that.
As I wrote in December, scientists applied evolutionary biology to find clues to how cholera–or, more precisely, the bacteria Vibrio cholerae– came to Haiti. They compared the DNA in the strain in Haiti to ones that have been found in other parts of the world. From this analysis, they drew a tree, which I’ve reprinted below.
The bacteria in Haiti was more closely related to strains in South Asia than ones from South America. So it was unlikely that cholera came to Haiti floating by water from a nearby country. The evolutionary tree led credence to idea that U.N. peacekeeping troops, some of whom came from Nepal, brought it with them by plane. An outbreak of cholera hit Nepal in September 2010, shortly before a battalion of Nepalese peacekeepers left for Haiti.
This analysis was a bit like a picture taken from 10,000 feet in the air. The bacteria that the scientists analyzed were just a small selection of the many strains that have made people sick over the past few decades. Notably missing from the tree were any bacteria from Nepal. That’s because those strains had not made their way into bacteria collections.
To get a picture up close–and to test the idea that U.N. peacekeepers brought cholera to Haiti–a team of Nepali, American, and Danish researchers collected 24 samples in Nepal at the end of last year. They sequenced the entire genomes of bacteria and compared them to the genomes of Haitian cholera. They reported their results today in the journal mBio.
And here’s their close-up tree. It clearly shows that the Haitian cholera strain evolved from one of four related lineages of V. cholerae circulating today in Nepal. It differs from the Nepalese strain by a single mutation.
It’s amazing that genome-sequencing methods have gotten so powerful that scientists can now use entire genomes to reconstruct an intercontinental outbreak. Yet ten months passed from the outbreak to the publication of this paper. In a blog at the mBio site, co-author Paul Keim explains why: politics. Governments can be reluctant to give up samples that might make them look bad. Building an evolutionary tree of a deadly outbreak takes more than data: it can take a lot of diplomacy, too.
Update: Martin Enserink, writing in Science, raises the question of whether the United Nations should compensate Haiti for the outbreak that this study now clearly lays at their doorstep. Hoo boy!
It’s time to revisit that grand old parasite, the brain-infecting Toxoplasma. The more we learn about it, the more marvelously creepy it gets.
Toxoplasma is a single-celled relative of the parasites that cause malaria. It poses a serious risk to people with compromised immune systems (for example, people with AIDS) and fetuses (which is why pregnant women need to avoid getting Toxoplasma infections). If you’ve got a healthy immune system, it doesn’t cause any immediate harm. (Ed Yong has explained why a purported link to brain cancer is very weak.) All told, perhaps a quarter or a third of all people on Earth carry thousands of Toxoplasma cysts in their heads. Most never become aware of their living cargo.
The Toxoplasma life cycle normally takes the parasite from cats to the prey of cats and back again. In the guts of cats, the parasites have sex and produce egg-like offspring which are shed with cat droppings. They can survive in soil for weeks or months. Rats and other mammals ingest the eggs, which produce cysts mainly in the brain. When the cats eat infected prey, they get infected.
For a little over ten years, scientists have been investigating whether Toxoplasma raises its odds of getting back into cats by manipulating their prey hosts. Oxford researchers kicked thing off by releasing healthy and infected rats into large enclosures. They spritzed corners of the enclosure with various odors, including the urine of rats, rabbits, and cats. Normally rats become anxious the instant they sniff cat urine and explore much less. Wise move.
Not so wise is the response of infected rats: in the enclosure experiments they either became indifferent to the smell of cats, or spent some extra time checking out the feline corner. There was no difference in how the infected rats responded to other smells.
Robert Sapolsky, a neuroscientist at Stanford University, and his colleagues have carried the experimental torch foreward. In 2006, they demonstrated just how precise Toxoplasma’s effects are. They found that infected rats did not lose their fear across the board. Dog urine still spooked them, and they could be trained to get scared of new stimuli. Only their innate fear of cats changed. Sapolsky’s team then looked at where the parasite actually ended up in the rat brain. They found Toxoplasma cysts clumped around the amygdala, a region of the brain that’s heavily involved in fear and other emotions.
Now Sapolsky and his colleagues have looked even closer at the parasite’s effects. They had rats sniff various odors and then examined their brains to look for a telltale protein called c-Fos. When neurons fire, they produce c-Fos, and so the more active a region of the brain, the more c-Fos accumulates in it. The scientists found two big differences in infected rat brains when they sniffed cat urine, both of which occurred in the region around the amygadala. A circuit in the brain that helps produce defensive behaviors became less active.
Near that circuit is another circuit that triggers sexual arousal.
And the parasite also altered this sexual arousal circuit. It increased the activity of those neurons.
Really, it would have been mind-blowing enough for a parasite to surgically swoop into a host brain and knock out the fear it felt towards a particular animal. We admirers of our parasite overlords would have been satisfied. But the possibility that these hosts are actually attracted to their enemy, that they feel the deepest desire a rat can feel, a desire that could lead them to death, and lead the parasite to live on, to achieve their own deepest sexual desires–well, we can only be grateful.