Our skin is encased in a snug microbial suit, from our scalps to the tips of our toes. Bacteria begin to colonize our skin from the moment we are born, and they continue to coat us throughout life. They do us many favors. They moisturize our skin to keep it supple; they unleash anti-microbial toxins to ward off pathogens that might make us ill. Scientists know that our skin is home to many species, but they can’t yet say exactly how many–or why some species are found more often on the elbow than on the chin.
Two years ago at a conference in North Carolina, I ran into Rob Dunn, a biologist who was conducting a survey of this menagerie. He was interested in the life found in one particular spot on the human body: the belly button. At the conference, he was handing out Q-tips people could use to swab their navels, which he and his colleagues could then study to tally up the species dwelling there.
Five months later, Dunn sent me a preliminary report: “You, my friend, are a wonderland.” I was the proud host of 53 different types of bacteria, including some decidedly weird creatures, such as a microbe only known from the ocean, and another from the soils of Japan.
I was only one of many human hosts to offer up our navel’s residents to Dunn’s scrutiny. Today, Dunn and his colleagues published a scientific paper on the biological diversity found in 60 bellybuttons in the journal PLOS One. They show that the diversity of my navel was not freakish. Even in a tiny divot of human flesh, dozens or even hundreds of species of bacteria can coexist. All told, Dunn and his colleagues identified 2368 different species living in our 60 belly buttons. The average person had 67 species, with the number ranging from a low of 29 species to a swarming high of 107.
Out of those 2368 species, the majority–1458–are new to science. A few of them are very common, while most are exquisitely rare. Dunn and his colleagues found that eight types of bacteria made up nearly half the microbes the scientists detected. Each of them was present on over seventy percent of us. But the vast majority of the species–2188 all told–lived on six or fewer people. Most were found only on a single individual.
It’s possible that the rare microbes are only visitors, dropping by for a short stay in our navels before dying out or traveling on. The most common species the scientists found may have long-term leases, having evolved adaptation that help them thrive in the bellybutton’s distinctive habitat. Dunn and his colleagues found that these abundant species were also closely related to each other compared to the rarer ones. It’s a pattern similar to the one found in rain forests, were only a few lineages of trees dominate, with many species only contributing a few trees. Your belly button, in other words, really is a jungle.
For more information, read Dunn’s account of the study.
P.S. I refer to these bacteria as belonging to “species.” It’s a convenient term but, when it comes to bacteria, not a precise one. Feel free to mentally substitute “operational taxonomic unit” or “phylotype.”
It’s getting close to two years now since a NASA-funded team of scientists announced they had found a form of life that broke all the rules by using arsenic to build its DNA. It’s become something of an obsession for me. If you want to follow the saga, click here and start back at the earliest post. In July I live-blogged the announcement that other scientists had replicated the experiment and failed to find the same results. In some ways, that was the logical end to the story
My fascination with this story has been tempered from the start by a creepy feeling. As a science writer, I most enjoy reporting on advances in biology: the research that opens up the natural world a little bit wider to our minds. The “#arseniclife” affair was less about biology than about how science gets done and the ways it goes wrong: the serious questions it raised about peer review, replication, and science communication. That fierce debate did some collateral damage. The microbe in question, known as GFAJ-1, went from being the species that would force us to rewrite the biology textbooks to yet another bacterium that offered no serious challenge to the uniformity of life. It became boring.
But biology is not boring. Elephants and redwoods may both be made of the same elements, may both build genes from DNA, may both use the same genetic code book to build proteins–but they’re very different from each other in some respects, and, each in their own way, are most certainly not boring. Neither is GFAJ-1. And so it’s a pleasure to see a new paper in the latest issue of Nature in which a group of scientists pick apart the biology of the microbe and discover something very interesting.
The whole search for arsenic life got its start because arsenic, despite being toxic, is very similar to an essential element, phosphorus. Phosphorus is part of the backbone of DNA, for example, and it is an ingredient in the energy-storing molecule ATP–in each case in a form known as phosphate, with four oxygen atoms tacked on. Arsenate (arsenic linked to three oxygen atoms) is just about identical in size, has a similar charge to its oxygen atoms, and has many other chemical similarities to phosphate.
So the arsenic life team wondered if life might be able to survive with arsenic instead of phosphorus. One way to test that idea would be to rocket off to a planet where there is only arsenic and no phosphorus and look for life. Another would be to look for life on Earth that can swap arsenic for phosphorus. The arsenic life team opted for the latter and headed to Mono Lake in California, the waters of which are loaded with arsenic. They brought a strain of bacteria back to their lab, weaned it off of phosphorus, and supplied it with arsenic instead. The bacteria still grew. That fact and other studies they conducted convinced them that the bacteria had, indeed, become arsenic life.
The consensus today is that the scientists unwittingly fed the bacteria just enough phosphorus to survive, and the tests that seemed to indicate the arsenic was inside the DNA weren’t executed carefully enough.
But think about that for a moment. Imagine what it’s like for a microbe in Mono Lake, or in the lab of a particularly sadistic scientist. You’re drowning in arsenate, and in order to stay alive, to keep growing, you need to grab the precious few phosphate molecules drifting by.
Dan Tawfik, an expert on protein function at the Weizmann Institute in Israel, and his colleagues have uncovered some of GFAJ-1′s secrets to survival. GFAJ-1 and other bacteria absorb phosphate through their outer membrane, into a sandwiched layer of fluid called the periplasm. Once there, the phosphate is grabbed by so-called phosphate binding proteins, which then deliver the phosphate to the interior of the microbe. Tawfik and his colleagues examined these proteins in unprecedented detail to see how they work.
The scientists offered the proteins a mixture of arsenate and phosphorus. Even when they raised the ratio to 500 molecules of arsenate to every phosphate molecule, the proteins still managed to pluck out phosphate over half the time. The scientists then examined the proteins to figure out how they make such fine discriminations. When the proteins encounter a molecule of phosphate, they enfold it in a tight pocket, which ties down the phosphate with 12 different hydrogen bonds. When arsenate falls into that pocket, it doesn’t quite fit in, and the bond between one of the oxygen atoms in the arsenate and one of the hydrogen atoms in the protein gets twisted. It gets pushed to such an uncomfortable angle that the arsenate drops out.
This finding suggests that ordinary microbes are well-adapted to picking out phosphates when they’re scarce, using their fussy phosphate binding proteins to reject abundant arsenate. GFAJ-1 is stuck in a place where phosphate is always scarce and arsenate is always dangerously copious. Tawfik and his colleagues found that one form of their phosphate binding proteins is spectacularly fussy, preferring phosphates by a factor of 4,500. What’s more, GFAJ-1 produces many copies of this super-fussy protein. As a result, GFAJ-1 can thrive in Mono Lake. In fact, it can handle arsenate-to-phosphate ratios up to 3,000 times higher than found in the lake.
Finding alien life on Earth would have been grand. But seeing how life as we know it manages to adapt to our planet’s extremes is also a pleasure. And it’s a good place for the story of arsenic life to stop: at the point where new science begins.
Rosie Redfield, the University of British Columbia microbiologist who became a leading skeptic of arsenic life, Maneesh points out in the comments that phosphates are actually abundant in Mono Lake. Thanks for pointing that out, Rosie Maneesh!]
In 1988, Richard Lenski, an evolutionary biologist now at Michigan State University, launched the longest running experiment on natural selection. It started with a single microbe–E. coli–which Lenski used to seed twelve genetically identical lines of bacteria. He placed each line in a separate flask, which he provisioned with a scant supply of glucose. The bacteria ate up the sugar in a few hours. The next day, he took a droplet of microbial broth from each flask and let it tumble into a new one, complete with a fresh supply of food. The bacteria boomed again, then starved again, and then were transferred again to a new home. Lenski and his colleagues have repeated this procedure every day for the past 24 years, rearing over 55,000 generations of bacteria.
I first reported on Lenski’s experiment 12 years ago, and since then I’ve revisited it every few years. The bacteria have been evolving in all sorts of interesting ways, and Lenski has been able to reconstruct the history of that evolution in great detail, thanks to a frozen fossil record. Every 500 generations Lenski and his students sock away some bacteria from each flask in a freezer. They can thaw out these ancestors whenever they wish and compare them to their youngest descendants. Biotechnology has improved drastically since 1988, giving Lenski an increasingly powerful evolutionary microscope. When he started out, it could take months to identify just one of the many mutations that arose in each lineage. These days, he and his colleagues can sequence an entire E. coli genome for a few hundred dollars and find every single new mutation in its DNA.
Four years ago, I wrote here about one particularly fascinating episode in the evolution going on in Lenski’s lab. It started in 2003, when the scientists there noticed something odd in one of the 12 flasks. It had become much more cloudy than the others. In a microbiology lab, that’s a sure-fire sign that the bacteria in a flask have experienced a population explosion.
At first the team suspected that some other species of bacteria had slipped into the flask and was breeding quickly. But they found that the flask was packed with E. coli—descendants of the original ancestor that Lenski had used to start the entire experiment. Somehow the bacteria in this one flask had evolved a way to grow much faster than the other bacteria.
The scientists determined that the bacteria had made a drastic switch: from feeding on the glucose to another compound, called citrate. Citrate is an ingredient in the broth where Lenski’s E. coli grows. It’s not food; instead, it helps keep the minerals in the broth in the right balance for E. coli to grow.
To a microbiologist, the emergence of E. coli that can eat citrate in a lab is deeply weird. E. coli typically can’t feed on citrate in the presence of oxygen. Some strains of E. coli can draw in citrate, but only if there’s no oxygen around. To make the reaction work, they have to pump out another compound called succinate at the same time. The ability of E. coli to feed on citrate in the presence of oxygen is extremely rare; it occurs when E. coli picks up the necessary genes from other species. In its normal environment (inside us), natural selection must not favor these mutants. Scientists have been studying E. coli in labs for over a century, making it the most intensely studied species, on Earth (as I explain in my book Microcosm). But in all that time, there has been only a single report of a citrate-feeding E. coli in a lab, back in 1982.
The inability of E. coli to grow on citrate is so stark, in fact, that microbiologists use it as a way to tell whether bacteria they come across are E. coli or not. It was thus a surprise to Lenski and his students to find a flask of E. coli suddenly feeding on citrate. The bacteria had not picked up the genes from another species. Instead, their new ability must have evolved after Lenski started his experiment with a single E. coli. This was not simply a case of natural selection enabling a species to do something better. This was a case of doing something new.
Zachary Blount–then a graduate student in Lenski’s lab and now a post-doctoral researcher there–led the investigation into this strange new development. Blount and his colleagues took away the glucose and found that the E. coli could thrive on citrate alone. They then defrosted the bacteria’s ancestors and fed them citrate to figure out when they acquired the ability. They found that a tiny fraction of the bacteria around generation 31,000 were able to grow very slowly on the citrate. Over a couple thousand generations, they got better at growing on citrate–so good, eventually, that they took over the flask and turned it cloudy.
Blount and Lenski first reported the evolution of the citrate-eaters in 2008. Now, after another four years of painstaking research, they’re back with a new paper that details what happened down at the molecular level. It’s a fascinating look at how new traits evolve by duplicating and recycling old parts.
The scientists found that the evolution took place in three chapters. In the first chapter, the stage was set for the transformation. In the second chapter, the bacteria became citrate feeders. And in the third chapter, they became much better citrate feeders.
It usually makes sense to start a story with Chapter One. But in this case, it’s better to start with Chapter Two: The Birth of the Citrate Feeders.
When E. coli finds itself in the absence of oxygen, it switches on a gene called citT. Like other species (including us), E. coli turns genes on and off by attaching proteins to short stretches of DNA nearby. When E. coli senses a lack of oxygen, proteins clamp onto one of these genetic switches near citT. Once they turn the gene on, it produces proteins that gets delivered to the surface of the cell. There they poke one end out into the environment and pull in citrate, while also pumping out succinate. After the citrate gets inside the microbe, the bacteria can chop it up to harvest its energy.
When E. coli is growing in oxygen, however, no proteins land on the genetic switch near the citT gene, and so it remains silent. The microbe wastes no energy making a protein that won’t help it grow.
Evolution has rewritten this little algorithm in the citrate eaters. As one cell in Lenski’s flask divided, it duplicated its DNA with one fateful mistake. It accidentally copied the citT twice. The new copy ended up near a different genetic switch–a switch that turns on neighboring genes in the presence of oxygen, not the absence.
While citT remained silent in the other bacteria in the flask, in the mutant cell, it switched on. The microbe began sticking citrate transporters on its surface and started drawing in the molecule. This mutation must have occurred by generation 31,500, when Blount found the earliest citrate eaters. The mutation was a crude hack; it produced a microbe that could draw in a little citrate, but not a lot. It still had to feed on glucose to get by.
Thus endeth Chapter Two.
In Chapter Three, life got better for the feeble citrate eaters. They copied the citT gene, along with its oxygen-switch promoter. Now the bacteria could make even more CitT channels, and thus pull in even more citrate. The bacteria made a third copy, and could pull in even more. Blount and his co-authors proved that the extra copies helped the bacteria this way by defrosting bacteria from Chapter Two and inserting copies of citT into them. Those early citrate eaters immediately got much better at feeding.
The scientists also found other mutations that arose during Chapter Three. While they have yet to figure out what those mutations did, the evidence they’ve gathered so far suggests the mutations allowed the bacteria to break down citrate more efficiently so they could get more energy from their food.
The most intriguing part of the story, however, is the first– Chapter One: Setting the Stage.
When Lenski and Blount first began to study the citrate eaters, they wondered what would happen if they wound back the evolutionary tape and let the bacteria re-evolve. Would the citrate feeding evolve again?
Blount thawed out ancestors from various moments in the history of the bacteria and started putting them through the same evolutionary experiment again. In some trials, the bacteria did indeed evolve into citrate eaters–but only if they came from after generation 20,000. This discovery suggested only after 20,000 generations were the bacteria prepared to evolve into citrate eaters. They must have already acquired other mutations that set the stage.
To test this idea, Blount and his colleagues thawed out some of the “prepared” bacteria: late-generation E. coli that had not yet gained mutations to citT. They created a miniature ring of DNA loaded with many copies of CitT and the oxygen-sensitive switch, and inserted it into the prepared bacteria. As they predicted, the bacteria now could suddenly feast magnificently on citrate.
But if Blount and his colleagues inserted the DNA ring into the original ancestor of the line, it grew poorly on citrate. That failure suggested that the early-generation bacteria were not ready to receive this evolutionary gift.
And thus a history takes shape:
Chapter One (from generaton zeo to at least generation 20,000): Our hero, E. coli, picks up mutations that don’t seem to have anything to do with feeding on citrate. They might have helped the bacteria grow better on their stingy rations of glucose. At least one of those mutations set the stage for feeding on citrate.
Chapter Two (around generation 31,500): The bacteria accidentally rewire their genome, so that a new copy of citT switches on in the presence of oxygen. Thanks to the mutations of Chapter One, this rewiring yields a modest but important improvement. Now the bacteria can feed a little on citrate, as well as on glucose.
Chapter Three (from about generation 31,500 to 33,000–and beyond): The bacteria make extra copies of the new and improved citT. They can pull in more citrate; new mutations fine-tune their metabolism to grow quickly on the molecule. World domination soon follows.
It’s remarkable how this experiment contains many elements of evolution that scientists have noted in other species. It’s common for genes to get duplicated, and for the new copy to be rewired for a new job. Snake venom, to pick one example, also evolved when genes were accidentally copied and then rewired. A gene that originally produced a digestive enzyme in the pancreas, for instance, now started making that enzyme in a snake’s mouth. It turned out to be a crude but effective venom. Later mutations fine-tuned the new venom gene until it became wickedly good.
The only important difference is that it took millions of years for snakes to evolve their arsenal of venoms, and scientists can only reconstruct their evolution by comparing living species. But in the case of E. coli, the transition unfolded fast enough for someone to track it from start to finish–and restart it when necessary.
Reference: Blount et al, “Genomic analysis of a key innovation in an experimental Escherichia coli population.” Nature, September 19 2012.
The world, it bears reminding, is far more complicated than what we can see. We take a walk in the woods and stop by a rotting log. It is decorated with mushrooms, and we faintly recall that fungus breaks down trees after they die. That’s true as far as it goes. But the truth goes much further. These days scientists do not have to rely on their eyes alone to observe the fungus on a log. They can drill into the wood, put the sawdust in a plastic bag, go to a lab, and fish the DNA out of the wood. A group of scientists did just this in Sweden recently, sequencing DNA from 38 logs in total. They published their results this week in the journal Molecular Ecology. In a single log, they found up to 398 species of fungi. Only a few species of fungi were living in all 38 logs; many species were limited to just one.
Consider that on your next walk in the woods. The one or two types of mushrooms you see on a log are an extroverted minority. The log is also filled with hundreds of other species that don’t make themselves known to you. Their invisible exuberance is a paradox. The fungi that live on rotting logs all make a living by releasing enzymes that break down wood. It’s puzzling that so many species can coexist in a log this way, instead of a single superior fungus.
The forces that drive up the diversity of fungi in a log are similar to the ones that fosterer the thousands of species of microbes in our bodies. For one thing, a log or a human body is not a uniform block of tissue. They both have geography. A microbe adapted to the acid bath of our stomach won’t fare well on the harsh desert of the skin. Likewise, what it takes to succeed as a fungus in a branch is different from what it takes in the heartwood of the trunk.
The human body changes over time, and a rotting log does, too. Babies are colonized by pioneer microbes, which alter the chemistry of their host and make it more welcoming to late-arriving species. The pioneers on a fallen log may include the spores of some species of fungi lurking in trees while they’re still alive. They burst into activity as soon as the tree crashes to the forest floor. Other species, delivered by the wind or snaking up through the soil, find it easier to infiltrate a log that’s already starting to rot. The early fungi may go after the easy sugar in the log, while later species unlock the energy in tougher tissues, like lignin and cellulose. Which particular pioneer starts to feed on a log first can make it inviting to certain species but not others.
Warfare also fosters diversity in a log. The fungi inside a log battle each other for food, spraying out chemicals that kill off their rivals. Each species has to balance the energy it puts into making enzymes to feed and weapons for war. Sometimes the war ends in victory for one species, but very often the result is a deadlock that leaves several species in an uneasy coexistence. There are more peaceful forces at work in a log, too. Many species of fungi in a log depend on each other. One species may feed on the waste produced by another, and supply another species with food in turn.
The world in a log influences the world as a whole. If it wasn’t for wood-rotting fungi, forests would be strewn with the durable remains of dead trees. When the first massive forests spread over the land 350 million years ago, fungi hadn’t yet adapted to decomposing logs. Instead of turning to soil, many trees ended up as coal. The great age of coal ended about 300 million years ago–right around the time that tree-rotting fungi emerged. Their emergence may have brought the age of coal to an end.
Three hundred million years later, that coal is coming back up to the surface of Earth to be burned. Some scientists are investigating fuels that could replace climate-warming ones like coal. One possibility is to pull out the energy-rich sugar locked up in the lignin and cellulose of crop wastes or switchgrass. On our own, we would not be able to perform the necessary alchemy. But fungi know how, and so scientists are sequencing the genomes of wood-rotting fungi to borrow their tricks. This is big-scale science: the genomes of over a dozen species have been sequenced or are in the sequencing pipeline. Yet a single log may contain twenty times more fungus genomes. At the moment, we can say for sure that the few mushrooms we see on a rotting log are far from its full reality. But it will be a long time before we know how all the parts of that reality fit together.
Next month, my first co-authored book is coming out. Evolution: Making Sense of Life is a textbook for biology majors, and my co-author is Doug Emlen, a professor at the University of Montana. I’ve heard many tales of disastrous collaborations between scientists and science writers, and so I don’t enter into them lightly. But working with Emlen has been a delight. No matter how many times we’ve had to rewrite a chapter, he threw himself into the work as if he was cannonballing into a swimming pool. And yet somehow Emlen was advancing his own research in evolutionary biology at the same time, quietly chugging away on some remarkable experiments. And today–just a week after we shipped our book off to the printers–Emlen’s latest, most intriguing paper has just come out in the journal Science.
If he wasn’t my co-author, I’d probably be writing about the new paper in the New York Times (or perhaps get into a bare-knuckle fight with the other reporters there for the right to do so). But given our connection, I’m going to use my blog to describe it.
When you’re a young evolutionary biologist, you’ve got to find creatures and questions that will sustain your career. Twenty years ago, Emlen realized that the perfect creatures for him would be horned beetles. In thousands of beetle species, the males grow enormous horns, which they use to battle each other for territories–be they tunnels, branches, or globs of sap. Often, male beetles will size each other up and not even bother challenging a beetle with a giant horn–because horns are a reliable signal of the good shape of a male beetle. These beetles embody Darwin’s original ideas about how sex could shape life. The competition for mates would favor mutations that enlarged the horn–not because it boosted the survival of beetles, but because it made male beetles more successful in the struggle for the chance to mate. (Terri Gross spoke to Emlen about beetles, and animal weapons in general, on Fresh Air.)
But there’s another way to contemplate a beetle’s horn. It develops as a beetle undergoes its metamorphosis from a larva into an adult. The mutations that build bigger horns must do so by altering the course of development. Until the late 1900s, the evolution of animal development was fairly mysterious, because scientists had no idea of which genes were involved in building emryos. But these days, that’s changed drastically. Emlen and I write about this at length in Evolution: Making Sense of Life, and online you can read about this field–”evo-devo”–over at the Understanding Evolution web site.
Emlen and his colleagues have discovered all sorts of intriguing things about the development of beetle horns. For example, big horns pull away precious resources from other parts of the developing beetle body. Male beetles with big horns have small eyes and antenna, Emlen has shown. This trade-off may put a limit on how big horns can get, since males with reduced eyes and other senses won’t fare well, even if they can battle any rival.
Beetles are hardly the only animals with sexual ornaments. Male widowbirds have long feathers, elk have huge antlers, and fiddler crabs have massive claws. One question that has occupied evolutionary biologists for decades is why these ornaments tend to be such reliable signals. If all it takes to scare off a rival beetle is a big horn, then it would make sense for weak beetles to shore up all their resources and build massive ornaments. Yet big ornaments continue to serve as trustworthy signals–as a warning to rival males and as an attraction for females.
In his new study, Emlen and his colleagues offer an evo-devo explanation for the link. As animals grow, two proteins play a major role: insulin and insulin-like growth factor (known as IGF). These hormones flow through the body, latch onto special receptors on cells, and trigger a series of chemical reactions that lead animals to grow faster. The amount of these proteins coursing through the body depends, in turn, on external factors such as how good the animal’s diet is. High insulin/IGF levels will spur an animal to develop a large body; in bad conditions, its body will be small. But individual animals vary in this response: in a good environment, the signals that some animals get from their insulin/IGF proteins make them grow bigger than other animals.
Emlen and his colleagues wondered if sexual ornaments were especially sensitive to the insulin/IGF signals. To find out, they turned to the aptly named rhinoceros beetles. The scientists injected molecules that blocked the insulin/IGF signal into rhinoceros beetle larvae just before they started to grow their horns.
Blocking the signal modestly stunted the bodies of the beetles. But it devastated the horns. Compared to the wings of the beetles, Emlen and his colleagues found, the horns were eight times more sensitive to manipulations of the insulin/IGF signals. (In this photo, the beetle on the right side has been injected with the insulin/IGF blocking molecules.)
The new study suggests that the exaggerated size of the beetle horns is unavoidably linked to the overall quality of a male. It grows in response to the same signals that control the entire body, but is more sensitive to them. There’s no way for weak males to cheat, because they can’t avoid using insulin/IGF signals to build a horn. If they have weak signals, they’ll produce a small horn.
And what goes for beetles may go for some other animals–or maybe a lot of other animals. When red deer stags grow new antlers, for example, the cells at the tips produce receptors for insulin/IGF. Emlen doesn’t touch on humans in the new paper, but the fact is that insulin/IGF signals are crucial in the transformation of boys to men, complete with big bones and muscles. Whether there’s a link in our species as there is in beetles is something I hope that we can report on in future editions of our book.
[Images: Doug Emlen]
[Note: This is the third of a four-part series
On Wednesday, I asked creationists for evidence. Over the past four days, I’ve been ordered to buy their book, offered it for free, invited to a debate and to guest blog. I’ve also been accused of lies and misdemeanors, of harrassing innocent creationists, and of being a duck. Actually, a hounding duck. But I still haven’t gotten my answer.
There is, of course, a lesson here.
Briefly, here’s the background. (For more details, read this post I wrote Thursday.) The Discovery Institute promotes intelligent design, which a Federal judge has declared “the progeny of creationism.” They have a staff, along with fellows, who write books (many of which are published by the Discovery Institute Press), run web sites, appear on cable TV, all to attack evolutionary biology and promote intelligent design. Their ranks include a few scientists (ie, people with Ph.D.’s who’ve published research in peer-viewed scientific journals), but in none of their published papers, to my knowledge, do they say anything like, “Our experiment thus provides clear evidence of intelligent design.” Instead, they make their big claims about intelligent design in their non-peer reviewed books and on their web sites. In 2005, the Discovery Institute set up an outfit called the Biologic Institute, where some scientists are supposedly doing the research that will show the world that Intelligent Design is the real deal. So far, they haven’t published any scientific papers in peer-reviewed journals to that effect.
On Wednesday, David Klinghoffer, the editor-in-chief of one of their sites, Evolution News and Views, published a piece promoting a new book from the Discovery Institute Press about human evolution, co-authored by two people from the Biologic Institute and one from the Discovery Institute. It was called, “A Veil Is Drawn Over Our Origin As Human Beings.” Along the way, Klinghoffer raised the issue of our fused chromosome, which, as I wrote Thursday, preserves clues to its origin as two separate chromosomes long ago. Klinghoffer claimed that the structure was not what you’d expect if the chromosome had fused six million years ago.
So here we have a claim. Scientific claims are based on evidence, or at least they should be. I wanted to know what the evidence was for this particular claim, but I couldn’t ask on Evolution News & Views (no comments allowed). So I went over to Facebook. There, the Biologic Institute has set up a page where they posted links to other web pages, one to including Klinghoffer’s page. And on Facebook, you have to let people comment. The biologist Nick Matzke was using the comments to set them straight with various lines of evidence about human evolution, which prompted the Biologic Institute to lay down a 100-word-or-less rule for comments. So I jumped in to ask–briefly–for the evidence about the claim about the human chromosome.
Whoever runs the Biologic Institute’s page responded by telling me to buy their new book. After all, as a book author myself, I wouldn’t just deliver the contents of my book to anyone who asked on my blog, would I?
Well, no, I replied. I then asked again, this time only requesting a citation to a paper that backed up their claim about the fused chromosome.
Now the Biologic Institute stopped replying. Other people left comments to let me know that they had read the book, and that the cited evidence amounted to nothing but a cherry-picked sentence from a ten-year-old paper. (Some of these comments have since been deleted.)
I asked the Biologic Institute if this account was true. Again, no answer.
Instead, I got an email from Klinghoffer himself. Rather than answer my question, he invited me to write a couple thousand-word pieces on Evolution News and Views as a debate with an unnamed co-authors. The debate would be on the various issues in the book. (Klinghoffer added that he wanted a debated focused on “ideas, not personalities.” This civility-minded person is the same guy who once wrote that one my blog posts was “preening and self-congratulatory.”) I hadn’t asked for such a debate, so I said no.
Instead, I asked again for the evidence. No answer.
Klinghoffer responded instead by publishing a piece on Evolution News and Views entitled, “We Called Out Darwinian Critic Carl Zimmer and He Folded.” Instead of answering my question, he condemned me for not reading the Discovery Institute’s book. “So you see what we’re up against,” he moaned. “Carl hasn’t read the book and now, having ducked out of a proper debate, he can go on denouncing it without ever having read it. He’s perfectly willing to waste our time on Facebook, where the phrase ‘pecked to death by ducks’ comes to mind.”
When the Biologic Institute posted a link to the piece on Facebook, I asked them again for an answer. No reply.
But David “Ideas Not Personalities” Klinghoffer was not through with me. The next day he returned to his comment-free platform to accuse me of “hounding our Biologic Institute colleagues on their Facebook page about a particular pet subject that he thinks he knows something about–chromosomal fusion at human chromosome two.”
Klinghoffer then got on Facebook to add a link to this piece on the Biologic Institute page. So I asked him my question again there. What is the evidence for the claim he made?
Again, nothing. By this point I had lost count of how many times I had asked the question.
Meanwhile, I put together this post to explain the latest research on the evolution of our fused chromosomes, from the world’s experts on primate genomes. By comparing the genomes of humans, chimpanzees, and gorillas, they could reconstruct what the original chromosomes were like, and how they evolved in each lineage–thanks to the kinds of mutations that scientists can see today in humans, as well as in many other species.
Unlike Klinghoffer, I let people comment on my posts. As of this writing, there are 70. A fair number of them claimed that intelligent design was the best explanation for our chromosomes. On Saturday, one of these commenters scoffed at the idea that mutations and evolutionary mechanisms could bring it about. If even just two mutations were required, I was out of luck.
Two? Again, I asked for the evidence. And this time I got an answer. I was directed to this 2008 paper in Genetics.
And this is why I ask for evidence. Because I can go do some research to see if the evidence holds up. The paper is a model, informed by experiments, of the rate at which mutations arise. It inspired another Discovery Institute fellow to claim it was evidence that evolution was too slow to have produced enough mutations in six million years to give rise to humans. And then the authors of the paper themselves wrote a letter to make it explicitly clear that the Discovery Institute was wrong. (Here’s a more recent paper that shows that the wait for mutations is not long, courtesy of another comment.)
On Saturday, I got another email from an Intelligent Design web site. This one is called Uncommon Descent. “We sponsor guest posts from people who disagre with us but are civil and well-informed on the issues,” wrote Denyse O’Leary. Would I want to write one?
I replied by pointing out that writing a guest blog post would be a redundant waste of time, since I had already asked my question many times over, and Uncommon Descent had actually just linked to my own blog post. I also found it strange that O’Leary would politely describe me as “civil and well-informed” in a message to me, when she had just written on Uncommon Descent that I am the sort of “Darwinist” who “only needs to pretend to know what they are talking about.”
Well, that little burst of politeness was fleeting indeed. Today, Uncommon Descent featured a new piece about me: “Carl Zimmer Doubles Down on Chromosome Two Lifes and Misdemeanors.”
Today’s attack comes from Discovery Institute fellow Cornelius Hunter. Hunter got a Ph.D. in biophysics at the University of Illinois, where he published three papers on protein structure a decade ago according to PubMed. Now he’s an adjunct professor at Biola University, an evangelical university in California.
Hunter claims that the evidence for a chromosome fusion in our ancestors only makes sense if we have already bought into the theory of evolution. It’s a long post that only gets around to what’s happened to the chromosomes at the very end.
The site of the fusion event on human chromosome number two does not provide an obvious picture of a past fusion event. There certainly are suggestions of such an event, but it is far from obvious as evolutionists claim.
Furthermore such an event, if it could survive, would have to take over the pre human population. In other words, the existing 48 chromosome population would have to die off. This is certainly not impossible, but there is no obvious reason why that would occur.
There are problems with the evidence. Perhaps the fusion event occurred, but the evidence carries nowhere near the certainty that evolutionists insist it does…
If evolution is not taken as an a priori, then these evidences are far less compelling. From this theory-neutral perspective, what is important is not reconciling chromosome counts or chimp-human chromosome similarities (after all, those are found throughout the respective genomes). What is important is the more direct evidence of a fusion event, such as in the region where the two chromosomes would fuse, and other tell-tale signs in the chromosome two.
Here the evidence is mixed. Certainly it is far less compelling than evolutionists ever tell their audiences. This need not be controversial. But it is.
That’s it. It’s not obvious. The evidence is mixed. How is it mixed? Hunter never says. What would be obvious evidence to him? He never says. What does he make of the latest research supporting the evolution of the fused chromosome? We have no idea. And–to sing the old refrain–what is the evidence for Klinghoffer’s claim? Hunter never says.
That’s where our story now stands. I’ll end this post the way this whole adventure began, with the question that has gone unanswered in so many, many ways:
An article on Evolution News & Views stated that the evidence for the fusion of human chromosome two “appears in a ‘degenerate,’ ‘highly diverged’ form that should not be the case if the joining happened in the recent past, circa 6 million years ago, as the Darwinian interpretation holds.” Where is the scientific evidence for this?
[Note: This post ended being the first of a series of four.
There’s something fascinating about our chromosomes. We have 23 pairs. Chimpanzees and gorillas, our closest living relatives, have 24. If you come to these facts cold, you might think this represented an existential crisis for evolutionary biologists. If we do indeed descend from a common ancestor with great apes, then our ancestors must have lost a pair after our lineage branched off, some six million years ago. How on Earth could we just give up an entire chromosome.
A close look at our genome and the genome of our close relatives reveals that we didn’t. We just combined a couple of them. Every now and then, chromosomes fuse. This fusion occurs as sperm and eggs develop, as pairs of chromosomes fold over each other and swap chunks of DNA. Sometimes two different chromosomes grab onto each other and then fail to separate.
Scientists have observed both humans and mammals with fused chromosomes. Chromosomes typically have distinctive stretches of DNA in their center and at their ends. From time to time, scientists will find an individual that’s short a chromosome, but one of the chromosomes it retains now has an odd structure, with chromosome endings near the middle and other peculiar features.
This might seem like a fantastic mutation–something like a human and a horse being joined into a centaur. Remarkably, however, fused chromosomes are real, and there are surprising number of normal, healthy people carrying them.
If humans and apes did indeed share a common ancestor, then it would make sense that two chromosomes fused in our ancestors. The rise of genome sequencing allowed them to test that hypothesis. They found that human chromosome two bears the hallmarks of an ancient chromosome fusion, with remnants of chromosome ends nestled at its core. In 2005, it became possible to test the hypothesis again, when a team of scientists sequenced the chimpanzee genome and could compare it to the human genome. The chimp genome team were able to match human chromosome two to two unfused chromosomes in the chimpanzee genome.
Ken Miller, a biologist at Brown who was an expert witness in the 2005 Dover creationism trial, includes this research in his lectures on evolution. Here’s a video of one of those lectures, where he lays out some of the evidence with impressive clarity.
What makes evolutionary biology such a fun subject to write about is that it does not stay still. While Miller’s description is entirely accurate, the past five years have rendered it obsolete. Last month, Evan Eichler at the University of Washington and his colleagues published a study in the journal Genome Research in which they deeper into the history of our missing chromosome.
They were able to do so thanks to the publication earlier this year of the gorilla genome. A comparison of the human, chimpanzee, and gorilla genomes confirms that the ancestors of gorillas branched off from the ancestors of chimpanzees and humans about ten million years ago. Humans and chimpanzees then branched apart later. A comparison between all three species provides a clearer picture of what our chromosomes looked like before they fused, and how they’ve changed since.
Eichler and his colleagues put together a diagram to illustrate this ten-million-year saga, which I’ve adapted here.
By comparing human chromosome two to the unfused versions in the chimpanzees and gorillas, Eichler and his colleagues reconstructed the chromosomes in the common ancestor of all three species:
The bands correspond to segments of each chromosome. The colors represent the two ancestral chromosomes (I’ll just call them green and red to keep from getting bogged down in confusing numbers). The hash marks represent regions of very unstable DNA. These areas, which are full of repeating sequences, are prone to accidentally getting duplicated, expanding the chromosome. They’re also where chromosomes are likely to trade chunks with other chromosomes. That’s why the red chromosome has a little green at the end. It had picked up part of the green chromosome earlier than the common ancestor of us, chimpanzees, and gorillas.
The green chromosome then changed:
Three key events are illustrated here. First, the top of the green chromosome flipped (another common type of mutation, called an inversion). Then a chunk of yet another chromosome got stuck to the end of the green chromosome, marked here in pink. And then a new piece of DNA got stuck at the end of the green chromosome, known as StSat, and marked here as a yellow dot.
The ancestors of gorillas then diverged from the ancestors of chimpanzees and humans. They underwent some ten million years of independent evolution, during which time a lot happened. For one thing, the cap on the green chromosome got duplicated and pasted onto other chromosomes, including the red one, and even on the other end of the green one itself. In the illustration below, the yellow and pink segments, along with the adjoining green segment, are represented by a brown oval:
The chromosomes at the right of the figure show you what our two chromosomes looked like before they got fused. When the human and chimpanzee lineages split, each lineage inherited them. And in each lineage, they evolved in a different way.
In the chimpanzee lineage, the chromosomes didn’t fuse. Instead, this happened:
And finally, here’s what happened to humans after our ancestors split from chimpanzees:
The two chromosomes fused, and the cap was deleted, inclusing StSat. It could no longer spread around our genome, the way it did in chimpanzees and gorillas.
This study is an important advance in our understanding of how human chromosomes evolved–a subject of medical significance, too, since the duplication of the DNA at the end of chromosomes can cause dangerous mutations that can cause genetic disorders. Plus, it is very cool to see how our chromosomes are, in fact, an ancient patchwork.
It just so happens that I came across this paper by a very roundabout way–but an instructive one. Over at the Panda’s Thumb, I learned yesterday that biologist Nick Matzke was trying to set things straight on a creationist Facebook page. The page is set up by an outfit called The Biologic Institute, which is promoting a new book by two of its employees that purports to reveal all the flaws in the evolutionary account of human beings. They linked to a post on a site run by the intelligent design clearinghouse, the Discovery Institute, which provided some details from the book. It’s called, “A Veil Is Drawn Over Our Origin as Human Beings,” and it’s written by David Klinghoffer.
Matzke left several comments explaining why they were wrong, and what some of the evidence for human evolution actually is. The Biologic Institute didn’t take this well: they suddenly announced that Facebook was not the appropriate venue for debate, and would limit comments to 100 words, or maybe shut the whole thing down.
I found this deliciously ironic and had to jump in too. I pointed out that the site they linked to does not allow comments (which is fairly typical of creationist web sites). So there was no other way to ask questions than to post them to Facebook. And my question concerned fused chromosomes.
The evidence from chromosomal fusion, for one, is strikingly ambiguous. In the Darwinian presentation, the fact that humans possess 23 chromosome pairs and great apes 24 clearly points to an event in which human chromosome 2 formed from a fusion, leaving in its wake the telltale sign of telomeric DNA — normally appearing as a protective cap at the end of the chromosome — in the middle where it doesn’t belong. Ergo, common descent.
But Casey [Luskin, of the Discovery Institute and co-author of the book] explains, there’s a lot wrong with this inference. Even if there was such an event and humans once had 24 chromosome pairs, it doesn’t at all follow that this happened in some prehuman past. Nothing stands in the way of picturing a human population bottleneck accomplishing the spread of a fused chromosome 2 from part of an early human community to all of it.
But the idea of such an event having occurred at all is itself far from sure. The telomeric DNA parked in the middle of chromosome 2 is not a unique phenomenon. Other mammals have it too, across their own genomes. Even if it were unique, there’s much less of it than you would expect from the amalgamation of two telomeres. Finally, it appears in a “degenerate,” “highly diverged” form that should not be the case if the joining happened in the recent past, circa 6 million years ago, as the Darwinian interpretation holds.
I was baffled, so I asked on Facebook for the evidence that the form of the chromosome wasn’t what you’d expect if it fused six million years ago.
What followed was a ridiculous runaround, some of which I’ll reproduce here:
Biologic Institute: Sorry, Carl, what link contains that particular quote?
Me: I am quoting from the page that YOU linked to.
Biologic Institute: Ah! That evidence is in the book that the post describes.
Carl Zimmer: In other words, the only way we can check these claims is to purchase the book? There’s no evidence published in peer-reviewed journals?
Carl Zimmer: The book you are pointing us to is written by two Biologic Institute employees–the same Institute that puts out this Facebook page. Why can’t you describe your evidence about the chromosome fusion here?
[An hour passes. No response.]
Carl Zimmer: Hello? Is anyone there? Are you choosing not to respond to my request for evidence from your own book? How do you calculate what the chromosome fusion DNA should look like if it fused six million years ago?
Biologic Institute: Carl, you write books for a living. Do you rehearse their content on your blog for anyone who asks?
Carl Zimmer: Hello, Biologic Institute. If I make a strong claim about science in an online forum, and someone asks me for evidence for that claim, I do not say, “Well, you’ll just have to read my book.” I provide the evidence–I point to the peer-reviewed research on which I based my statement. But, hey, I’d be perfectly satisfied if you pointed me to a scientific paper that presents calculations showing that the chromosome fusion could not have happened six million years ago. I can go find it for myself–if such a paper actually exists.
Well, that was the last I heard from the Biologic Institute. They still haven’t piped back up on their own thread. However, I did hear from someone who had read the book, Paul MacBride. (He even reviewed it here.) Here’s the comment he left on Facebook:
Carl, I can tell you the answer to your question, as I have read the book. Luskin provides no evidence for this. Well, more correctly, he quotes a question from this paper http://www.ncbi.nlm.nih.gov/pubmed/12421751 “If the fusion occurred within the telomeric repeat arrays less than ∼6 Mya, why are the arrays at the fusion site so degenerate?” but not their three suggested answers. Luskin asserts that if a chromosomal fusion occurred it should have been a neat and tidy joining of the two chromosomes in question, anything else is a Problem For Evolution. Dave Wisker addressed this succintly in a comment at Panda’s Thumb http://pandasthumb.org/archives/2012/07/paul-mcbrides-r.html#comment-288503
That paper MacBride mentions? It’s the 2002 paper I mentioned at the start, the one that presented evidence for fusion based on a study of the human genome. In other words, the authors of this new intelligent design book cherry-pick a quote out of a paper that’s ten years old (you can check for yourself, the paper’s free). That, it seems, is all the evidence they have. If anyone tells you how impressive the science is behind intelligent design, how superior it is to evolutionary biology, may I suggest you use this example to show them how wrong they are.
I read the 2002 paper long ago, but MacBride’s link led me to reread it. I also noticed that it was cited by a number of more recent papers, including Eichler’s new one. It just goes to show how you can end up learning something new in the most unexpected places.
Update #2: Actually, they’ll do a lot more–here’s my round up of the four days since I posted this.
We all started out as a fertilized egg: a solitary cell about as wide as a shaft of hair. That primordial sphere produced the ten trillion cells that make up each of our bodies. We are not merely sacs of identical cells, of course. A couple hundred types of cells arise as we develop. We’re encased in skin, inside of which bone cells form a skeleton; inside the skull are neurons woven into a brain.
What made this alchemy possible? The answer, in part, is viruses.
Viruses are constantly swarming into our bodies. Sometimes they make us sick; sometimes our immune systems vanquish them; and sometimes they become a part of ourselves. A type of virus called a retrovirus makes copies of itself by inserting its genes into the DNA of a cell. The cell then uses those instructions to make the parts for new viruses. HIV makes a living this way, as do a number of viruses that can trigger cancer.
On rare occasion, a retrovirus may infect an egg. Now something odd may happen. If the egg becomes fertilized and gives rise to a whole adult individual, all the cells in its body will carry that virus. And if that individual has offspring, the virus gets carried down to the next generation.
At first, these so-called endogenous retroviruses lead a double life. They can still break free of their host and infect new ones. Koalas are suffering from one such epidemic. But over thousands of years, the viruses become imprisoned. Their DNA mutates, robbing them of the ability to infect new hosts. Instead, they can only make copies of their genes that are then inserted back into their host cell. Copy after copy build up the genome. To limit the disruption these viruses can cause, mammals produce proteins that can keep most of them locked down. Eventually, most endogenous retroviruses mutate so much they are reduced to genetic baggage, unable to do anything at all. Yet they still bear all the hallmarks of viruses, and are thus recognizable to scientists who sequence genomes. It turns out that the human genome contains about 100,000 fragments of endogenous retroviruses, making up about eight percent of all our DNA.
Evolution is an endlessly creative process, and it can turn what seems utterly useless into something valuable. All the viral debris scattered in our genomes turns out to be just so much raw material for new adaptations. From time to time, our ancestors harnessed virus DNA and used it for our own purposes. In a new paper in the journal Nature, a scientist named Samuel Pfaff and a group of fellow scientists report that one of those purposes to help transform eggs into adults.
In their study, Pfaff and his colleagues at the Salk Institute for Biological Sciences examined fertilized mouse eggs. As an egg starts to divide, it produces new cells that are capable of becoming any part of the embryo–or even the membrane that surrounds the embryo or the placenta that pipes in nutrients from the animal’s mother. In fact, at this early stage, you can pluck a single cell from the clump and use it to grow an entire organism. These earliest cells are called totipoent.
After a few days, the clump becomes a hollowed out ball. The cells that make the ball up are still quite versatile. Depending on the signals a cell gets at this point, it can become any cell type in the body. But once the embryo reaches this stage, its cells have lost the ability to give rise to an entirely new organism on their own, because they can’t produce all the extra tissue required to keep an embryo alive. Now the cells are called pluripotent. The descendants of pluripotent cells gradually lose their versatility and get locked into being certain types of cells. Some become hematopoetic cells, which can turn into lots of different kinds of blood cells but can no longer become, say, skin cells.
Pfaff and his colleagues examined mouse embryos just after they had divided into two cells, in the prime of their totipotency. They catalogued the genes that were active at that time–genes which give the cells their vastly plastic potential. They found over 100 genes that were active at the two-cell stage, and which then shut down later on, by the time the embryo had become a hollow ball.
One way cells can switch genes on and off is producing proteins that latch onto nearby stretches of DNA called promoters. The match between the protein and the promoter has to be precise; otherwise, genes will be flipping on at all the wrong times, and failing to make proteins when they’re needed. Pfaff and his colleagues found that all the two-cell genes had identical promoters–which would explain how they all managed so become active at the same time.
What was really remarkable about their discover was the origin of those promoters. They came from viruses.
During the earliest stage of the embryo’s development, these virus-controlled genes are active. Then the cells clamp down on them, just as they would clamp down on viruses. Once those genes are silenced, the totipotent cells become pluripotent.
Pfaff and his colleagues also discovered something suprising when they looked at the pluripotent ball of cells. From time to time, the pluripotent cells let the virus-controlled genes switch on again, and then shut them back down. All of the cells, it turns out, cycle in and out of what the scientists call a “magic state,” in which they become temporarily totipotent again. (The pink cells in this photo are temporarily in that magic state.)
Cells in the magic state can give rise to any part of the embryo, as well as the placenta and other tissue outside the embryo. Once the virus-controlled genes get shut down again, they lose that power. This discovery demonstrated that these virus-controlled genes really are crucial for making cells totipotent.
Pfaff and his colleagues propose that the domestication of these virus promoters was a key step in the evolution of mammals with placentas. The idea that viruses made us who were are today may sound bizarre, except that Pfaff is hardly the first person to find evidence for it. Last year, for example, I wrote about how placental mammals stole a virus protein to build the placenta.
A discovery this strange inevitably raises questions that its discoverers cannot answer. What are the virus-controlled genes doing in those first two cells? Nobody knows. How did the domestication of this viral DNA help give rise to placental mammals 100 million years ago? Who knows? Why are viruses so intimately involved in so many parts of pregnancy? Awesome question. A very, very good question. Um, do we have any other questions?
We don’t have to wait to get all the answers to those questions before scientists can start to investigate one very practical application of these viruses. In recent years, scientists have been reprogramming cells taken either from adults or embryos, trying to goose them back into an early state. By inducing cells to become stem cells, the researchers hope to develop new treatments for Parkinson’s disease and other disorders where defective cells need to be replaced. Pfaff suggests that we should switch on these virus-controlled genes to help push cells back to a magic state.
If Pfaff’s hunch turns out to be right, it would be a delicious triumph for us over viruses. What started out as an epidemic 100 million years ago could become our newest tool in regenerative medicine.
(For more on these inner passengers, see my book A Planet of Viruses.)
[Image: Courtesy Salk Institute.]
In the past few weeks, there’s been a string of horrific tales of cannibalism and other zombie-esque behavior in the news. How to explain a handful of reports of people doing the unspeakable? One answer circulating around these days is that it must be parasites. And for some journalists, the question demands a call to the Centers for Disease Control to find out what they’re hiding from us!
1. Andy Campbell of the Huffington Post asked the CDC if some kind of zombie virus was to blame for the recent attacks. On June 1, he reported on HuffPo’s Politics page the following scoop:
“CDC does not know of a virus or condition that would reanimate the dead (or one that would present zombie-like symptoms),” wrote agency spokesman David Daigle in an email to The Huffington Post.
The Huffington Post entitled Campbell’s hard-hitting investigation, “Zombie Apocalypse: CDC Denies Existence Of Zombies Despite Cannibal Incidents.” That’s perhaps the finest deployment of the word despite in the history of journalism.
The story, by the way, received 65,797 likes on Facebook.
2. The Daily Caller picked up Campbell’s expose later that day, essentially reposting his whole piece. But Daily Caller reporter Michael Bastasch also salted his cut-and-paste with a few pieces of his own research. For example, Bastasch reports, some people “have claimed it was caused by the LBQ-79 virus.”
The Daily Caller headline: “CDC: No zombies, despite cannibal attacks.”
Can’t those pointy-headed government pencil-pushers see what’s in front of their own dismembered noses???
3. Andy Campbell must have bitten Michael Bastasch’s ear, because the idea of parasite-induced zombification has infected the editorial offices of the Daily Caller. On June 4, a minute before midnight, Josh Peterson, Tech Editor at the Daily Caller, posted a new story:
Clearly, this story could not wait for the morning, presumably because zombies prowl the night.
Here’s how last night’s story starts:
The Centers for Disease Control and Prevention (CDC) recently denied knowing of “a virus or condition that would reanimate the dead (or one that would present zombie-like symptoms),” after a series of instances of cannibalism across the country were reported, but remains silent about the effect of zombie-inducing parasites that live in human brains.
The parasite is Toxoplasma gondii. Lifting material reported here at Discover, Peterson describes how Toxoplasma alters rat behavior, reducing their fear of cats, the final host for the parasite. About one in five humans carries Toxoplasma too, as do many mammals, including pigs.
Now–watch as Peterson makes an Olympic-quality pivot off of the pig and back into the horde of zombies:
While pigs are known to engage in cannibalism, no known correlation between the parasite and cannibalism has been found.
France also has a high prevalence of Toxoplasma-infected people.
The Daily Caller’s inquiry to the CDC about why it omitted parasites from its denial, and about the possibility of the cannibals having been infected by the Toxoplasma, however, was met with silence.
Silence! Perhaps the CDC spokespeople simply couldn’t pick up their phones, because they were busy holding their heads in their hands, wondering how their clever zombie attack survival guide had gotten them into this mess, and how they’re going to get out of it.
As someone who has written a lot about the sinister powers of parasites, I’d be right in the thick of it to report on any genuine information on a zombie-parasite outbreak–if there was one. But there isn’t. While some people may laugh off these “reports” from the Daily Caller or the Huffington Post, others may take them–or subsequent rumors–seriously. So let me just lay out the reality of what parasites can do to the brain:
1. Some parasites do control the brains of their hosts. There are viruses and fungi that drive their insect hosts to the tops of plants, so that the parasites can shower down on new hosts, for example. Some flatworms that infect fish cause them to thrash around at the surface of the water, to make them easier pickings for birds, inside of which the flatworms can reproduce. Parasitic wasps rob cockroaches of their will, so that the wasps can lay eggs on them, which then invade their docile host. Other parasitic wasps turn their hosts into bodyguards. After they emerge from caterpillars, their dying hosts fight off other insects that would try to eat the pupating wasps. It’s important to note that the most extreme examples of host manipulation come from tiny-brained animals such as insects or fish–not people.
2. A cannibalistic zombie is no benefit to a parasite. Host manipulation generally shows all the signs of natural selection at work. Mutations to genes in the parasites gradually give them the ability to alter the behavior of their host more and more, in ways that boost the odds that the parasite will be able to reproduce. But what possible good could come from a parasite that caused its host to kill other people? That just robs you (the parasite) of a potential host. Not smart. And so it should come as no surprise that scientists have never found a parasite that causes cannibalism. (Tasmanian devils spread cancer to each other by biting each other’s faces, but they don’t need cancer’s help to get into fights. The cancer cells just go along for the aggressive ride.)
3. Fine, but what about rabies? The rabies virus is pretty creepy, both in its manipulation of its host and in its deadliness. You get rabies from the saliva of an infected animal that bites you, and the virus then slips into the nervous system. Rabies infection makes animals aggressive–and thus more likely to bite new victims. The horror of rabies infection has haunted us for thousands of years (for more, check out the wonderful book, Rabies: A Cultural History of the World’s Most Diabolical Virus by Bill Wasik and Monica Murphy, coming out next month. Wasik, an editor at Wired, sent me the book a few months back, and I loved it.)
But the reality is that rabies does not produce armies of human zombies trying to bite other people. It is possible to get infected by someone’s saliva, but it’s an extremely rare occurrence. We humans are a dead end for the virus. It depends on other animals to continue circulating from host to host.
And, again, let’s think this through. Rabies is 100% deadly unless you get treated. But it stays in circulation because its hosts remain alive long enough to bite other animals before they die. Dismembering a victim and eating him for dinner, or chewing off his face under a Florida overpass are not going to do a virus much good.
4. But what about the LBQ-79 virus? I read about it on the Daily Caller! Couldn’t that be a rabies-like virus that makes people cannibalistic zombies? There is no such thing.
5. But there is such a thing as Toxoplasma, right? Absolutely. Toxoplasma is one of my favorite parasites. And there’s a lot of evidence now that it can influence human behavior–albeit in subtle ways. Kathleen McAuliffe lays out the current science nicely in this story in the March issue of the Atlantic.
But again, let’s work through this. Toxoplasma only alters its animal hosts to make them easier prey for the parasite’s final host. All effects on humans seem to be pale shadows of that strategy. (And, just like rabies, we are a dead end for Toxoplasma.) So how do we get from making your host easy prey to becoming a zombie cannibal?
Also, bear in mind that the parasite dwells in the brains of over a billion people. It’s been there for centuries, if not thousands of years. Only now is it suddenly turning people into cannibals? No self-respecting science-fiction scriptwriter would try pitching that idea to Hollywood. Unfortunately, the editors at the Daily Caller have lower standards than that.
[Update: I originally wrote that Bastasch was the author of the second Daily Caller story. Fixed. Also, I accidentally block quoted some of my own text, giving the impression it was in the Daily Caller. Fixed.]
[Second update, 5:10 pm: On Twitter, Peterson responded to this post by writing, "Nice piece, but why'd you leave out the parts about it being related to mental disorders?" and, later asking, "So you're content in not explaining the effect of the parasite on the brain in your piece, then?"
In case I wasn't clear enough by linking to McAuliffe's story, let me be clear now: a number of studies suggest that an exposure to Toxoplasma may influence people's personality. It has also been identified as a risk factor for schizophrenia. Here's one recent review in Developmental Neurobiology that presents evidence of a raised risk in people who were exposed before birth. (Other studies have found that other infections can also raise the risk.)
But I find Peterson baffling. Is he suggesting that we can explain an outbreak of cannibalism by pre-birth exposure to Toxoplasma, leading decades later to schizophrenia, leading to cannibalism? If so, it's not only ridiculous, but it's insulting to the 2 million people who suffer from schizophrenia in the United States, as well as their families.]