Your hands are, roughly speaking, 360 million years old. Before then, they were fins, which your fishy ancestors used to swim through oceans and rivers. Once those fins sprouted digits, they could propel your salamander-like ancestors across dry land. Fast forward 300 million years, and your hands had become fine-tuned for manipulations: your lemur-like ancestors used them to grab leaves and open up fruits. Within the past few million years, your hominin ancestors had fairly human hands, which they used to fashion tools for digging up tubers, butchering carcasses, and laying the groundwork for our global dominance today.
We know a fair amount about the transition from fins to hands thanks to the moderately mad obsession of paleontologists, who venture to inhospitable places around the Arctic where the best fossils from that period of our evolution are buried. (I wrote about some of those discoveries in my first book, At the Water’s Edge.)
By comparing those fossils, scientists can work out the order in which the fish body was transformed into the kind seen in amphibians, reptiles, birds, and mammals–collectively known as tetrapods. Of course, all that those fossils can preserve are the bones of those early tetrapods. Those bones were built by genes, which do not fossilize. Ultimately the origin of our hands is a story of how those fin-building genes changed, but that’s a story that requires more evidence than fossils to tell.
A team of Spanish scientists has provided us with a glimpse of that story. They’ve tinkered with the genes of fish, and turned their fins into proto-limbs.
Before getting into the details of the new experiment, leap back with me 450 million years ago. That’s about the time that our early vertebrate ancestors–lamprey-like jawless fishes–evolved the first fins. By about 400 million years ago, those fins had become bony. The fins of bony fishes alive today–like salmon or goldfish–are still built according to the same basic recipe. They’re made up mostly of a stiff flap of fin rays. At the base of the fin, they contain a nubbin of bone of the sort that makes up our entire arm skeleton (known as endochondral bone). Fishes use muscles attached to the endochondral bone to maneuver their fins as they swim.
Our own fishy ancestors gradually modified this sort of fin over millions of years. The endochondral bone expanded, and the fin rays shrank back, creating a new structure known as a lobe fin. There are only two kinds of lobe fin fishes left alive today: lungfishes and coelacanths. After our ancestors split off from theirs, our fins became even more limb like. The front fins evolved bones that corresponded in shape and position to our ulna and humerus.
A 375-million-year-old fossil discovered in 2006, called Tiktaalik, had these long bones, with smaller bones at the end that correspond to our wrist. But it still had fin rays forming fringe at the edges of its lobe fin. By 360 million years ago, however, true tetrapods had evolved: the fin rays were gone from their lobe fins, and they had true digits. (The figure I’m using here comes from my more recent book, The Tangled Bank.)
Both fins and hands get their start in embryos. As a fish embryo grows, it develops bumps on its sides. The cells inside the bumps grow rapidly, and a network of genes switches on. They not only determine the shape that the bump grows into, but also lay down a pattern for the bones which will later form.
Scientists have found that many of the same genes switch on in the limb buds of tetrapod embryos. They’ve compared the genes in tetrapod and fish embryos to figure out how changes to the gene network turned one kind of anatomy into the other.
One of the most intriguing differences involves a gene known as 5′Hoxd. In the developing fish fin, it produces proteins along the outer crest early on in its development. The proteins made from the gene then grab other genes and switch them on. They switch on still other genes, unleashing a cascade of biochemistry.
Back when you were an embryo, 5′Hoxd also switched on early in the development of your limbs. It then shut off, as it does in fish. But then, a few days later, it made an encore performance. It switched back on along the crest of the limb bud a second time. This second wave of 5′Hoxd marked a new pattern in your limb: it set down the places where your hand bones would develop.
Here, some scientists proposed, might be an important clue to how the hand evolved. It was possible that mutations in our ancestors caused 5′Hoxd to turn back on again late in development. As a result, it might have added new structures at the end of its fins.
If this were true, it would mean that some of the genetic wherewithal to build a primitive hand was already present in our fishy ancestors. All that was required was to assign some genes to new times or places during development. Perhaps, some scientists speculated, fishes today might still carry that hidden potential.
Recently Renata Freitas of Universidad Pablo de Olavide in Spain and her colleagues set out to try to unlock that potential. They engineered zebrafish with an altered version of the 5′Hoxd gene, which they could switch on whenever they wanted by dousing a zebrafish embryo with a hormone.
The scientists waited for the fishes to start developing their normal fin. The fishes expressed 5′Hoxd at the normal, early phase. The scientists waited for the gene to go quiet again, as the fins continued to swell. And then they spritzed the zebrafish with the hormone. The 5′Hoxd gene switched on again, and started making its proteins once more.
The effect was dramatic. The zebrafish’s fin rays became stunted, and the end of its fin swelled with cells that would eventually become endochondral bone.
These two figures illustrate this transformation. The top figure here looks down at the back of the fish. The normal zebrafish is to the left, and the engineered one is to the right. The bottom figure provides a close-up view of a fin. The blue ovals are endochondral bone, and the red ones display a marker that means they’re growing quickly.
One of the most interesting results of this experiment is that this single tweak–a late boost of 5′Hoxd–produces two major effects at once. It simultaneously shrinks the outer area of the fin where fin rays develop and expands the region where endochondral bone grows. In the evolution of the hand, these two changes might have occurred at the same time.
It would be wrong to say that Freitas and her colleagues have reproduced the evolution of the hand with this experiment. We did not evolve from zebrafishes. They are our cousins, descending from a common ancestor that lived 400 million years ago. Ever since that split, they’ve undergone plenty of evolution, adapting to their own environment. As a result, a late boost of 5′Hoxd was toxic for the fishes. It interfered with other proteins in the embryos, and they died.
Instead, this experiment provides a clue and a surprise. It provides some strong evidence for one of the mutations that turned fins into tetrapod limbs. And it also offers a surprise: after 400 million years, our zebrafish cousins still carry some of the genetic circuits we use to build our hands.
Freitas et al, “Hoxd13 Contribution to the Evolution of Vertebrate Appendages.” Developmental Cell dx.doi.org/10.1016/j.devcel.2012.10.015
Schneider and Shubin, “Making Limbs from Fins.” Developmental Cell dx.doi.org/10.1016/j.devcel.2012.11.011
For all the progress scientists have made in studying Neanderthals since then, the answer remains tough–in part because it’s not that easy to define a species.
NOVA asked me to write about this enduring question. You can read my answer here.
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.
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]
Here’s a video of a great talk about the evolution of whales that anatomist Joy Reidenberg gave at the recent PopTech conference. You may have seen her on the show Inside Nature’s Giants. Here’s my profile of Reidenberg this spring in the New York Times, in which I focused on what it’s like to take apart whales for a living.
[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.
As I’ve mentioned a couple times, I’ve been working for a couple years with biologist Douglas Emlen on a new textbook about evolution, intended for biology majors. It’s scheduled to be published next month, and we’ve gathered some gratifying endorsements. Here are a selection:
“Exciting is a word not often used to describe a new textbook. But, by using powerful examples, beautiful images, and finely wrought prose Zimmer and Emlen have produced a text that not only conveys the explanatory power of evolution, but one permeated with the joy of doing science. Their text can only be described as an exciting moment for our field: it is an important accomplishment for our students and for evolutionary biology at large.” –Neil Shubin, University of Chicago, author of Your Inner Fish.
“A richly illustrated and very clearly written text, Evolution: Making Sense of Life brings forth the excitement, power, and importance of modern evolutionary biology in an accessible, yet sophisticated overview of the field.” –Sean B. Carroll, University of Wisconsin, Madison, author of Endless Forms Most Beautiful.
“If there was ever a book that makes it obvious why evolution is a fascinating topic—and a topic that goes to the core of understanding what biology is about—this is it. It truly makes you better understand and appreciate the biological world around us.” –Svante Paabo, Director, Max Planck Institute for Evolutionary Anthropology
“Two master craftsmen in the art of scientific communication have combined to produce an excellent basic text on evolution: it informs, explains, teaches and inspires. The illustrations are outstanding.” –Peter R. Grant, Princeton University
“Carl Zimmer and Douglas Emlen have captured in this stunning new book the excitement and richness of twenty-first century evolutionary biology. They describe clearly and elegantly not only what, but also how, we are learning about evolutionary processes and the patterns they produce. The writing is compelling, the illustrations beautiful and truly informative, and the balance between breadth and depth of discussion on each topic just right. This is a book that would make anyone think about becoming an evolutionary biologist today.” –John N. Thompson, University of California, Santa Cruz
“Beautifully written and lavishly illustrated, here’s a superb textbook that can do double duty gracing the coffee table. This book is bound to attract many more students into the field of evolutionary biology.” –Richard Lenski, Michigan State University
“This is not your grandmother’s evolution text. Breathtakingly illustrated, this book covers not only the usual topics in evolution – adaptation, drift, phylogenetic analysis – but also a host of new and exciting areas where groundbreaking research is occurring.” –Marlene Zuk, University of Minnesota
You can pre-order the book on Amazon here. And here is information at the web site at our publisher, Roberts & Company. Excitingly, they are also creating an iPad version of the book, with many interactive features. The app itself is free, and you can use it to download the first chapter (also free). The remaining chapters will be rolling out soon, with the price to be determined later. (No Android version, I’m afraid!)
After half a year of stormy debate, we are finally getting to see all the gory details about how two teams of scientists produced some disturbing flu viruses. I’ve written about this unfolding story previously here, at Slate, here again, in the New York Times, and back here again.
In tomorrow’s New York Times, I step back and take a look at the two published studies, and talk to experts about what those studies do–and don’t–tell us about how likely we are to face a new flu pandemic in the years to come. There’s still a huge amount about the flu that we don’t know yet, sorry to say. Check it out. (I also spoke with Times editor Michael Mason on this week’s science podcast. Listen here.)
This month has seen a flood of new studies and reviews on the microbiome, the collection of creatures that call our bodies home. In tomorrow’s New York Times, I look at why scientists are going to so much effort to map out these 100 trillion microbes.
The microbiome is not just an opportunistic film of bugs: it’s an organ that play an important part in our well-being. It starts to form as we’re born, develops as we nurse, and comes to maturity like other parts of the body. It stabilizes our immune system, keeps our skin intact, synthesizes vitamins, and serves many other functions. Yet the microbiome is an organ made up of thousands of species–an ecosystem, really. And so a number of scientists are calling for a more ecological view of our health, rather than simply trying to wage warfare against infections.