More creationist misconceptions about the eye

Jonathan Sarfati, a particularly silly creationist, is quite thrilled — he’s crowing about how he has caught Richard Dawkins in a fundamental error. The eye did not evolve, says Sarfati, because it is perfectly designed for its function, and Dawkins’ suggestion that there might be something imperfect about it is wrong, wrong, wrong. He quotes Dawkins on the eye.

But I haven’t mentioned the most glaring example of imperfection in the optics. The retina is back to front.

Imagine a latter-day Helmholtz presented by an engineer with a digital camera, with its screen of tiny photocells, set up to capture images projected directly on to the surface of the screen. That makes good sense, and obviously each photocell has a wire connecting it to a computing device of some kind where images are collated. Makes sense again. Helmholtz wouldn’t send it back.

But now, suppose I tell you that the eye’s ‘photocells’ are pointing backwards, away from the scene being looked at. The ‘wires’ connecting the photocells to the brain run over all the surface of the retina, so the light rays have to pass through a carpet of massed wires before they hit the photocells. That doesn’t make sense…

What Dawkins wrote is quite correct, and nowhere in his refutation does Sarfati show that he is wrong. Instead, Sarfati bumbles about to argue against an argument that no biologist makes, that the eye is a poor instrument for detecting patterns of light. The argument is never that eyes do their job poorly; it’s that they do their job well, by a peculiar pattern of kludgy patches to increase functionality that bear all the hallmarks of a long accumulation of refinements. Sarfati is actually supporting the evolutionary story by summarizing a long collection of compromises and odd fixes to improve the functionality of the eye.

There’s a fundamental question here: why does the vertebrate eye have its receptors facing backwards in the first place? It is not the best arrangement optically; Sarfati is stretching the facts to claim that God designed it that way because it was superior. It ain’t. The reason lies in the way our eye is formed, as an outpocketing of the cortex of the brain. It retains the layered structure of the cortex, even; it’s the way it is because of how it was assembled, not because its origins are rooted in optical optimality. You might argue that it’s based on a developmental optimum, that this was the easiest, simplest way to turn a light-sensitive patch into a cup-shaped retina.

Evolution has subsequently shaped this patch of tissue for better acuity and sensitivity in certain lineages. That, as I said, is a product of compromises, not pre-planned design. Sarfati brings up a series of odd tweaks that make my case for me.

  1. The vertebrate photoreceptors are nourished and protected by an opaque layer called the retinal pigmented epithelium (RPE). Obviously, you couldn’t put the RPE in front of the visual receptors, so the retina had to be reversed to allow it to work. This is a beautiful example of compromise: physiology is improved at the expense of optical clarity. This is exactly what the biologists have been saying! Vertebrates have made a trade-off of better nutrient supplies to the retina for a slight loss of optical clarity.

  2. Sarfati makes the completely nonsensical claim that the presence of blood vessels, cells, etc. in the light path do not compromise vision at all because resolution is limited by diffraction at the pupil, so “improvements of the retina would make no difference to the eye’s performance”. This is clearly not true. The fovea of the vertebrate eye represents an optimization of a small spot on the retina for better optical properties vs. poorer circulation: blood vessels are excluded from the fovea, which also has a greater density of photoreceptors. Obviously, improvements to the retina do make a difference.

    It’s also not a condition that is universal in all vertebrates. Most birds, for instance, do not have a vascularized retina — there is no snaky pattern of blood vessels wending their way across the photoreceptors. Birds do have greater acuity than we do, as well. What birds have instead is a strange structure inside their eye called the pecten oculi, which looks kind of like an old steam radiator dangling into the vitreous humor, which seems to be a metabolic specialization to secrete oxygen and nutrients into the vitreous to supply by diffusion the retina.

  3. Sarfati also plays rhetorical games. This is a subtly dishonest argument:

    In fact, cephalopods don’t see as well as humans, e.g. no colour vision, and the octopus eye structure is totally different and much simpler. It’s more like ‘a compound eye with a single lens’.

    First, there’s a stereotype he’s playing to: he’s trying to set up a hierarchy of superior vision, and he wants our god-designed eyes at the top, so he tells us that most cephalopods have poorer vision than we do. He doesn’t bother to mention that humans don’t have particularly good vision ourselves; birds have better eyes. So, is God avian?

    That business about the cephalopod being like a compound eye is BS; if it’s got a single lens, it isn’t a compound eye, now is it? It’s also again pandering to a bias that our eyes must be better than mere compound eyes, since bugs and other lowly vermin have those. Cephalopods have rhabdomeric eyes, meaning that their photoreceptors have a particular structure and use a particular set of biomolecules in signal transduction, but that does not in any way imply that they are inferior. In fact, they have some superior properties: the cephalopod retina is tightly organized and patterned, with individual rhabdomeres ganged together into units called rhabdomes that work together to process light. Their ordered structure means that cephalopods can detect the polarity of light, something we can’t do at all. This is a different kind of complexity, not a lesser one. They can’t see color, which is true, but we can’t sense the plane of polarity of light in our environment.

    I must also note that the functions of acting as a light guide (more below) and using pigment to shield photoreceptors are also present in the cephalopod eye…only by shifting pigments in supporting cells that surround the rhabdome, rather than in a solid RPE. Same functions, different solutions, the cephalopod has merely stumbled across a solution that does not simultaneously impede the passage of light.

    Color vision, by the way, is a red herring here. Color is another compromise that has nothing to do with the optical properties of the arrangement of the retina, but is instead a consequence of biochemical properties of the photoreceptors and deeper processing in the brain. If anything, color vision reduces resolution (because individual photoreceptors are tuned to different wavelengths) and always reduces sensitivity (you don’t use color receptors at night, you may have noticed, relying instead on rods that are far less specific about wavelength). But if he insists, many teleosts have a greater diversity of photopigments and can see colors we can’t even imagine…so humans are once again also-rans in the color vision department.

  4. Sarfati is much taken with the discovery that some of the glial cells of the eye, the Müller cells, act as light guides to help pipe light through the tangle of retinal processing cells direct to the photoreceptors. This is a wonderful innovation, and it is entirely true that in principle this could improve the sensitivity of the photoreceptors. But again, this would not perturb any biologist at all — this is what we expect from evolution, the addition of new features to overcome shortcomings of original organization. If we had a camera that clumsily had the non-optical parts interposed between the lens and the light sensor, we might be impressed with the blind, clumsy intricacy of a solution that involved using an array of fiber optics to shunt light around the opaque junk, but it wouldn’t suggest that the original design was particularly good. It would indicate short-term, problem-by-problem debugging rather than clean long-term planning.

  5. Sarfati cannot comprehend why the blind spot would be a sign of poor design, either. He repeats himself: why, it’s because the eye needs a blood supply. Yes, it does, and the solution implemented in our eyes is one that compromises resolution. I will again point out that the cephalopod retina also needs a blood supply, and they have a much more elegant solution; the avian eye also needs a blood supply, but is not invested with blood vessels. He gets very circular here. The argument is not that the vertebrate eye lacks a solution to this problem, but that there are many different ways to solve the problem of organizing the retina with its multiple demands, and that the vertebrate eye was clearly not made by assembling the very best solutions.

Sarfati really needs to crawl out of his little sealed box of creationist dogma and discover what scientists actually say about these matters, and not impose his bizarre creationist interpretations on the words of people like Dawkins and Miller. What any comparative biologist can see by looking at eyes across multiple taxa is that they all work well enough for their particular functions, but they all also have clear signs of assembly by a historical process, like evolution and quite unlike creation, and that there is also evidence of shortcomings that have acquired workarounds, some of which are wonderfully and surprisingly useful. What we don’t see are signs that the best solutions from each clade have been extracted and placed together in one creature at the pinnacle of creation. And in particular — and this has to be particularly grating to the Genesis-worshipping creationists of Sarfati’s ilk, since he studiously avoids the issue — Homo sapiens is not standing alone at that pinnacle of visual excellence. We’re kinda straggling partway down the peak, trying to compensate for some relics of our ancestry, like the fact that we’re descended from nocturnal mammals that let the refinement of their vision slide for a hundred million years or thereabouts, while the birds kept on optimizing for daylight acuity and sensitivity.

Now we’ve got some big numbers to throw around, too

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Only ours are methodologically valid. It’s a common creationist tactic to fling around big numbers to ‘disprove’ evolution: for instance, I’ve had this mysterious Borel’s Law (that anything with odds worse than 1 in 1050 can never happen) thrown in my face many times, followed by the declaration that the odds of the simplest organism forming by chance are 1 in 10340,000,000. It’s complete nonsense, of course — their calculations all ignore the reality of the actual events, assuming that everything must form spontaneously and all at once, which is exactly the opposite of how probability plays a role in evolution. It’s annoying and inane, and the creationists never seem to learn…perhaps because the rubes they pander to are easily dazzled by even bogus mathematics, so they keep doing it.

We’re going to have to start firing back. Doug Theobald, a long-time contributor to Talk.Origins and the Panda’s Thumb, has written a very nice paper testing the likelihood that all life on earth is not related by common descent, and he comes up with some numbers of many digits to support evolutionary theory. Nick Matzke has a summary, and the story has been written up for National Geographic.

Basically, the idea is this: take a small set of known, conserved proteins that are shared in all organisms, not restricting ourselves to one kingdom or one phylum, but grabbing them all. In this paper, that data set consists of 23 proteins from 12 taxa in the Big Three domains: Bacteria, Archaea, and Eukarya. Then set up many different models to explain the relationships of these species. For instance, you could organize them into the classic single tree, where all are related, or you could model them as three independent origins, for each of Bacteria, Archaea, or Eukarya, or you could postulate other combinations, such as that Bacteria arose independently of Archaea and Eukarya, which share a common ancestor. Finally, you tell your computer to do a lot of statistics on the models, asking how likely it is that two independent groups would each arrive at similar sequences, rating each of the models for parsimony and accuracy against the evidence.

And the winner is…common ancestry, with one branching tree! This is what we expected, of course, and what Theobald has done is to test our assumptions, always a good thing to do.

More complicated permutations of these models were also tried. What if there were a significant amount of horizontal gene transfer? Would that make multiple origins of modern life more likely? He was testing models like the ones below, where the dotted lines represent genes that leap across taxa to confuse the issue.

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The answer here is that they don’t. These models can also be evaluated by statistical methods, and the best fit is again the one on the right, with a single ancestral root. People might recall the infamous “Darwin was wrong” cover from New Scientist—well, these results say that New Scientist was wrong, the existence of extensive horizontal gene transfer does not negate the fact of common descent.

So what’s the big number? There are lots of them in the paper, since it evolves many comparisons, but Theobald distills it down to just the odds that bacteria have an independent origin from Archaea and eukaryotes:

But, based on the new analysis, the odds of that are “just astronomically enormous,” he said. “The number’s so big, it’s kind of silly to say it”–1 in 10 to the 2,680th power, or 10 followed by 2,680 zeros.

One in 102680? Hey, aren’t those odds a little worse than Borel’s criterion of one in 1050?

Stay tuned to the Panda’s Thumb. Apparently, once he finishes up the trifling business of wrapping up a semester’s teaching, Theobald will be putting up a synopsis of his own and answering questions online.

Theobald D (2010) A formal test of the theory of universal common ancestry. Nature 465(13):219-222.

Neandertal!

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You don’t have to tell me, I know I’m late to the party: the news about the draft Neandertal genome sequence was announced last week, and here I am getting around to it just now. In my defense, I did hastily rewrite one of my presentation to include a long section on the new genome information, so at least I was talking about it to a few people. Besides, there is coverage from a genuine expert on Neandertals, John Hawks, and of course Carl Zimmer wrote an excellent summary. All I’m going to do now is fuss over a few things on the edge that interested me.

This was an impressive technical feat. The DNA was extracted from a few bone fragments, and it was grossly degraded: the average size of a piece of DNA was less than 200 base pairs, much of that was chemically degraded, and 95-99% of the DNA extracted was from bacteria, not Neandertal. An immense amount of work was required to filter noise from the signal, to reconstruct and reassemble, and to avoid contamination from modern human DNA. These poor Neandertals had died, had rotted thoroughly, and the bacteria had worked their way into almost every crevice of the bone to chew up the remains. All that was left were a few dead cells in isolated lacunae of the bone; their DNA had been chopped up by their own enzymes, and death and chemistry had come to slowly break them down further.

Don’t hold your breath waiting for the draft genome of Homo erectus. Time is unkind.

We have to appreciate the age of these people, too. The oldest Neandertal fossils are approximately 400,000 years old, and the species went extinct about 30,000 years ago. That’s a good run; as measured by species longevity, Homo sapiens neandertalensis is more successful than Homo sapiens sapiens. We’re going to have to hang in there for another 200,000 years to top them.

The samples taken were from bones found in a cave in Vindija, Croatia. Full sequences were derived from these three individuals, and in addition, some partial sequences were taken from other specimens, including the original type specimen found in the Neander Valley in 1856.

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Samples and sites from which DNA was retrieved. (A) The three bones from Vindija from which Neandertal DNA was sequenced. (B) Map showing the four archaeological sites from which bones were used and their approximate dates (years B.P.).

The three bones used for sequencing were directly dated to 38.1, 44.5, and 44.5 thousand years ago, which puts them on the near end of the Neandertal timeline, and after the likely time of contact between modern humans and Neandertals, which probably occurred about 80,000 years ago, in the Middle East.

Just for reference: these samples are 6-7 times older than the entire earth, as dated by young earth creationists. The span of time just between the youngest and oldest bones used is more than six thousand years old, again, about the same length of time as the YEC universe. Imagine that: we see these bone fragments now as part of a jumble of debris from one site, but they represent differences as great as those between a modern American and an ancient Sumerian. I repeat once again: the religious imagination is paltry and petty compared to the awesome reality.

A significant revelation from this work is the discovery of the signature of interbreeding between modern humans and Neandertals. When those humans first wandered out of the homeland of Africa into the Middle East, they encountered Neandertals already occupying the land…people they would eventually displace, but at least early on there was some sexual activity going on between the two groups, and a small number of human-Neandertal hybrids would have been incorporated into the expanding human population—at least, in that subset that was leaving Africa. Modern European, Asian, and South Pacific populations now contain 1-4% Neandertal DNA. This is really cool; I’m proud to think that I had as a many-times-great grandparent a muscular, beetle-browed big game hunter who trod Ice Age Europe, bringing down mighty mammoths with his spears.

However, it is a small contribution from the Neandertals to our lineage, and it’s not likely that these particular Neandertal genes made a particularly dramatic effect on our ancestors. They didn’t exactly sweep rapidly and decisively through the population; it’s most likely that they are neutral hitch-hikers that surfed the wave of human expansion. Any early matings between an expanding human subpopulation and a receding Neandertal population would have left a few traces in our gene pool that would have been passively hauled up into higher numbers by time and the mere growth of human populations. In a complementary fashion, any human genes injected into the Neandertal pool would have been placed into the bleeding edge of a receding population, and would not have persevered. No uniquely human genes were found in the Neandertals examined, but we can’t judge the preferred direction of the sexual exchanges in these encounters, though, because any hybrids in Neandertal tribes were facing early doom, while hybrids in human tribes were in for a long ride.

Here’s the interesting part of these gene exchanges, though. We can now estimate the ancestral gene sequence, that is, the sequences of genes in the last common ancestor of humans and Neandertals, and we can ask if there are any ‘primitive’ genes that have been completely replaced in modern human populations by a different variant, but Neandertal still retained the ancestral pattern (see the red star in the diagram below). These genes could be a hint to what innovations made us uniquely human and different from Neandertals.

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Selective sweep screen. Schematic illustration of the rationale for the selective sweep screen. For many regions of the genome, the variation within current humans 0 is old enough to include Neandertals (left). Thus, for SNPs in present-day humans, Neandertals often carry the derived -1 allele (blue). However, in genomic regions where an advantageous mutation arises (right, red star) and sweeps to high frequency or fixation in present-day humans, Neandertals will be devoid of derived alleles.

There’s good news and bad news. The bad news is that there aren’t very many of them: a grand total of 78 genes were identified that have a novel form and that have been fixed in the modern human population. That’s not very many, so if you’re an exceptionalist looking for justification of your superiority to our ancestors, you haven’t got much to go on. The good news, though, is that there are only 78 genes! This is a manageable number, and represent some useful hints to genes that would be worth studying in more detail.

One other qualification, though: these are 78 genes that have changes in their coding sequence. There are also several hundred other non-coding, presumably regulatory, sequences that are unique to humans and are fixed throughout our population. To the evo-devo mind, these might actually be the more interesting changes, eventually…but right now, there are some tantalizing prospects in the coding genes to look at.

Some of the genes with novel sequences in humans are DYRK1A, a gene that is present in three copies in Down syndrome individuals and is suspected of playing a role in their mental deficits; NRG3, a gene associated with schizophrenia, and CADPS2 and AUTS2, two genes associated with autism. These are exciting prospects for further study because they have alleles unique and universal to humans and not Neandertals, and also affect the functioning of the brain. However, let’s not get confused about what that means for Neandertals. These are genes that, when broken or modified in modern humans, have consequences on the brain. Neandertals had these same genes, but different forms or alleles of them, which are also different from the mutant forms that cause problems in modern humans. Neandertals did not necessarily have autism, schizophrenia, or the minds of people with Down syndrome! The diseases are just indications that these genes are involved in the nervous system, and the differences in the Neandertal forms almost certainly caused much more subtle effects.

Another gene that has some provocative potential is RUNX2. That’s short for Runt-related transcription factor 2, which should make all the developmental biologists sit up and pay attention. It’s a transcription factor, so it’s a regulator of many other genes, and it’s related to Runt, a well known gene in flies that is important in segmentation. In humans, RUNX2 is a regulator of bone growth, and is a master control switch for patterning bone. In modern humans, defects in this gene lead to a syndrome called cleidocranial dysplasia, in which bones of the skull fuse late, leading to anomalies in the shape of the head, and also causes characteristic defects in the shape of the collar bones and shoulder articulations. These, again, are places where Neandertal and modern humans differ significantly in morphology (and again, Neandertals did not have cleidocranial dysplasia — they had forms of the RUNX2 gene that would have contributed to the specific arrangements of their healthy, normal anatomy).

These are tantalizing hints to how human/Neandertal differences could have arisen—by small changes in a few genes that would have had a fairly extensive scope of effect. Don’t view the many subtle differences between the two as each a consequence of a specific genetic change; a variation in a gene like RUNX2 can lead to coordinated, integrated changes to multiple aspects of the phenotype, in this case, affecting the shape of the skull, the chest, and the shoulders.

This is a marvelous insight into our history, and represents some powerful knowledge we can bring to bear on our understanding of human evolution. The only frustrating thing is that this amazing work has been done in a species on which we can’t, for ethical reasons, do the obvious experiments of creating artificial revertants of sets of genes to the ancestral state — we don’t get to resurrect a Neandertal. With the tools that Pääbo and colleagues have developed, though, perhaps we can start considering some paleogenomics projects to get not just the genomic sequences of modern forms, but of their ancestors as well. I’d like to see the genomic differences between elephants and mastodons, and tigers and sabre-toothed cats…and maybe someday we can think about rebuilding a few extinct species.

Green RE, Krause J, Briggs AW, Maricic T, Stenzel U, Kircher M, Patterson N, Li H, Zhai W, Fritz MH, Hansen NF, Durand EY, Malaspinas AS, Jensen JD, Marques-Bonet T, Alkan C, Prüfer K, Meyer M, Burbano HA, Good JM, Schultz R, Aximu-Petri A, Butthof A, Höber B, Höffner B, Siegemund M, Weihmann A, Nusbaum C, Lander ES, Russ C, Novod N, Affourtit J, Egholm M, Verna C, Rudan P, Brajkovic D, Kucan Z, Gusic I, Doronichev VB, Golovanova LV, Lalueza-Fox C, de la Rasilla M, Fortea J, Rosas A, Schmitz RW, Johnson PL, Eichler EE, Falush D, Birney E, Mullikin JC, Slatkin M, Nielsen R, Kelso J, Lachmann M, Reich D, Pääbo S. (2010) A draft sequence of the Neandertal genome. Science 328(5979):710-22.

The secret life of babies

Years ago, when the Trophy Wife™ was a psychology grad student, she participated in research on what babies think. It was interesting stuff because it was methodologically tricky — they can’t talk, they barely respond in comprehensible way to the world, but as it turns out you can get surprisingly consistent, robust results from techniques like tracking their gaze, observing how long they stare at something, or even the rate at which they suck on a pacifier (Maggie, on The Simpsons, is known to communicate quite a bit with simple pauses in sucking.)

There is a fascinating article in the NY Time magazine on infant morality. Set babies to watching puppet shows with nonverbal moral messages acted out, and their responses afterward indicate a preference for helpful agents and an avoidance of hindering agents, and they can express surprise and puzzlement when puppet actors make bad or unexpected choices. There are rudiments of moral foundations churning about in infant brains, things like empathy and likes and dislikes, and they acquire these abilities untaught.

This, of course, plays into a common argument from morality for religion. It’s unfortunate that the article cites deranged dullard Dinesh D’Souza as a source — is there no more credible proponent of this idea? That would say volumes right there — but at least the author is tearing him down.

A few years ago, in his book “What’s So Great About Christianity,” the social and cultural critic Dinesh D’Souza revived this argument [that a godly force must intervene to create morality]. He conceded that evolution can explain our niceness in instances like kindness to kin, where the niceness has a clear genetic payoff, but he drew the line at “high altruism,” acts of entirely disinterested kindness. For D’Souza, “there is no Darwinian rationale” for why you would give up your seat for an old lady on a bus, an act of nice-guyness that does nothing for your genes. And what about those who donate blood to strangers or sacrifice their lives for a worthy cause? D’Souza reasoned that these stirrings of conscience are best explained not by evolution or psychology but by “the voice of God within our souls.”

The evolutionary psychologist has a quick response to this: To say that a biological trait evolves for a purpose doesn’t mean that it always functions, in the here and now, for that purpose. Sexual arousal, for instance, presumably evolved because of its connection to making babies; but of course we can get aroused in all sorts of situations in which baby-making just isn’t an option — for instance, while looking at pornography. Similarly, our impulse to help others has likely evolved because of the reproductive benefit that it gives us in certain contexts — and it’s not a problem for this argument that some acts of niceness that people perform don’t provide this sort of benefit. (And for what it’s worth, giving up a bus seat for an old lady, although the motives might be psychologically pure, turns out to be a coldbloodedly smart move from a Darwinian standpoint, an easy way to show off yourself as an attractively good person.)

So far, so good. I think this next bit gives far too much credit to Alfred Russel Wallace and D’Souza, though, but don’t worry — he’ll eventually get around to showing how they’re wrong again.

The general argument that critics like Wallace and D’Souza put forward, however, still needs to be taken seriously. The morality of contemporary humans really does outstrip what evolution could possibly have endowed us with; moral actions are often of a sort that have no plausible relation to our reproductive success and don’t appear to be accidental byproducts of evolved adaptations. Many of us care about strangers in faraway lands, sometimes to the extent that we give up resources that could be used for our friends and family; many of us care about the fates of nonhuman animals, so much so that we deprive ourselves of pleasures like rib-eye steak and veal scaloppine. We possess abstract moral notions of equality and freedom for all; we see racism and sexism as evil; we reject slavery and genocide; we try to love our enemies. Of course, our actions typically fall short, often far short, of our moral principles, but these principles do shape, in a substantial way, the world that we live in. It makes sense then to marvel at the extent of our moral insight and to reject the notion that it can be explained in the language of natural selection. If this higher morality or higher altruism were found in babies, the case for divine creation would get just a bit stronger.

No, I disagree with the rationale here. It is not a problem for evolution at all to find that humans exhibit an excessive altruism. Chance plays a role; our ancestors did not necessarily get a choice of a fine-tuned altruism that works exclusively to the benefit of our kin — we may well have acquired a sloppy and indiscriminate innate tendency towards altruism because that’s all chance variation in a protein or two can give us. There’s no reason to suppose that a mutation could even exist that would enable us to feel empathy for cousins but completely abolish empathy by Americans for Lithuanians, for instance, or that is neatly coupled to kin recognition modules in the brain. It could be that a broad genetic predisposition to be nice to fellow human beings could have been good enough to favored by selection, even if its execution caused benefits to splash onto other individuals who did not contribute to the well-being of the possessor.

But that idea may be entirely moot, because there is some evidence that babies are born (or soon become) bigoted little bastards who do quickly cobble up a kind of biased preferential morality. Evolution has granted us a general “Be nice!” brain, and also that we acquire capacities that put up boundaries and foster a kind of primitive tribalism.

But it is not present in babies. In fact, our initial moral sense appears to be biased toward our own kind. There’s plenty of research showing that babies have within-group preferences: 3-month-olds prefer the faces of the race that is most familiar to them to those of other races; 11-month-olds prefer individuals who share their own taste in food and expect these individuals to be nicer than those with different tastes; 12-month-olds prefer to learn from someone who speaks their own language over someone who speaks a foreign language. And studies with young children have found that once they are segregated into different groups — even under the most arbitrary of schemes, like wearing different colored T-shirts — they eagerly favor their own groups in their attitudes and their actions.

That’s kind of cool, if horrifying. It also, though, points out that you can’t separate culture from biological predispositions. Babies can’t learn who their own kind is without some kind of socialization first, so part of this is all about learned identity. And also, we can understand why people become vegetarians as adults, or join the Peace Corps to help strangers in far away lands — it’s because human beings have a capacity for rational thought that they can use to override the more selfish, piggy biases of our infancy.

Again, no gods or spirits or souls are required to understand how any of this works.

Although, if they did a study in which babies were given crackers and the little Catholic babies all made the sign of the cross before eating them, while all the little Lutheran babies would crawl off to make coffee and babble about the weather, then I might reconsider whether we’re born religious. I don’t expect that result, though.

Everything old is new again

If you’ve ever invited me out to give a science talk, you know that what I generally talk about is this concept of deep homology: the discovery that features that we often consider the hallmarks of complex metazoan life often have at their core a network of genetic circuitry that was first pioneered in bacteria. What life has done is taken useful functional elements that were worked out in the teeming, diverse gene pools of the dominant single-celled forms of life on earth and repurposed it in novel ways. The really interesting big bang of life occurred long before the Cambrian, as organisms evolved useful tools for signaling, adhesion, regulation, and so forth — all stuff that was incredibly useful for a single cell negotiating through space and time in a complex external environment, and which could be coopted for building multicellular organisms.

But if you don’t feel like flying me out to tell you all about it, Carl Zimmer has an excellent article on deep homology in the NYT, and he uses a new example I’ll have to steal: a genetic module that we use to regulate blood vessel growth that can also be found in yeast cells, where it is used to maintain cell walls.

Design flaws support evolution

This is a nicely done lecture on design flaws in our anatomy and physiology, to refute claims of intelligent design.

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I know exactly how creationists will reply, though, since I’ve heard it often enough. She’s making a theological argument, they’ll say, claiming to know God’s intent and making an assumption of his goals. It will be a restatement of the old chestnut, “God works in mysterious ways.”

However, that’s not the argument here. Imperfections and sub-optimal properties are an outcome of evolutionary theory; this is a positive argument that observations of the world best fit a model positing a history of accidents and refinements constrained along lines of descent. If the creationists want to complain, they first have to propose a set of predictions that would discriminate between accident and design, and starting from a god who can do anything at any whim is not a fruitful source of hypotheses.

How to make a snake

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First, you start with a lizard.

Really, I’m not joking. Snakes didn’t just appear out of nowhere, nor was there simply some massive cosmic zot of a mutation in some primordial legged ancestor that turned their progeny into slithery limbless serpents. One of the tougher lessons to get across to people is that evolution is not about abrupt transmutations of one form into another, but the gradual accumulation of many changes at the genetic level which are typically buffered and have minimal effects on the phenotype, only rarely expanding into a lineage with a marked difference in morphology.

What this means in a practical sense is that if you take a distinct form of a modern clade, such as the snakes, and you look at a distinctly different form in a related clade, such as the lizards, what you may find is that the differences are resting atop a common suite of genetic changes; that snakes, for instance, are extremes in a range of genetic possibilities that are defined by novel attributes shared by all squamates (squamates being the lizards and snakes together). Lizards are not snakes, but they will have inherited some of the shared genetic differences that enabled snakes to arise from the squamate last common ancestor.

So if you want to know where snakes came from, the right place to start is to look at their nearest cousins, the lizards, and ask what snakes and lizards have in common, that is at the same time different from more distant relatives, like mice, turtles, and people…and then you’ll have an idea of the shared genetic substrate that can make a snake out of a lizard-like early squamate.

Furthermore, one obvious place to look is at the pattern of the Hox genes. Hox genes are primary regulators of the body plan along the length of the animal; they are expressed in overlapping zones that specify morphological regions of the body, such as cervical, thoracic, lumbar, sacral/pelvic, and caudal mesodermal tissues, where, for instance, a thoracic vertebra would have one kind of shape with associated ribs, while lumbar vertebra would have a different shape and no ribs. These identities are set up by which Hox genes are active in the tissue forming the bone. And that’s what makes the Hox genes interesting in this case: where the lizard body plan has a little ribless interruption to form pelvis and hindlimbs, the snake has vertebra and ribs that just keep going and going. There must have been some change in the Hox genes (or their downstream targets) to turn a lizard into a snake.

There are four overlapping sets of Hox genes in tetrapods, named a, b, c, and d. Each set has up to 13 individual genes, where 1 is switched on at the front of the animal and 13 is active way back in the tail. This particular study looked at just the caudal members, 10-13, since those are the genes whose expression patterns straddle the pelvis and so are likely candidates for changes in the evolution of snakes.

Here’s a summary diagram of the morphology and patterns of Hox gene expression in the lizard (left) and snake (right). Let’s see what we can determine about the differences.

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Evolutionary modifications of the posterior Hox system in the whiptail lizard and corn snake. The positions of Hox expression domains along the paraxial mesoderm of whiptail lizard (32-40 somites, left) and corn snake (255-270 somites, right) are represented by black (Hox13), dark grey (Hox12), light grey (Hox11) and white (Hox10) bars, aligned with coloured schemes of the future vertebral column. Colours indicate the different vertebral regions: yellow, cervical; dark blue, thoracic; light blue, lumbar; green, sacral (in lizard) or cloacal (in snake); red, caudal. Hoxc11 and Hoxc12 were not analysed in the whiptail lizard. Note the absence of Hoxa13 and Hoxd13 from the corn snake mesoderm and the absence of Hoxd12 from the snake genome.

The morphology is revealing: snakes and lizards have the same regions, cervical (yellow), thoracic (blue), sacral (or cloacal in the snake, which lacks pelvic structures in most species) in green, and caudal or tail segments (red). The differences are in quantity — snakes make a lot of ribbed thoracic segments — and detail — snakes don’t make a pelvis, usually, but do have specializations in that corresponding area for excretion and reproduction.

Where it really gets interesting is in the expression patterns of the Hox genes, shown with the bars that illustrate the regions where each Hox gene listed is expressed. They are largely similar in snake and lizard, with boundaries of Hox expression that correspond to transitions in the morphology of vertebrae. But there are revealing exceptions.

Compare a10/c10 in the snake and lizard. In the snake, these two genes have broader expression patterns, reaching up into the thoracic region; in the lizard, they are cut off sharply at the sacral boundary. This is interesting because in other vertebrates, the Hox 10 group is known to have the function of suppressing rib formation. Yet there they are, turned on in the posterior portion of the thorax in the snake, where there are ribs all over the place.

In the snake, then, Hox a10 and c10 have lost a portion of their function — they no longer shut down ribs. What is the purpose of the extended domain of a10/c10 expression? It may not have one. A comparison of the sequences of these genes between various species reveals a detectable absence of signs of selection — the reason these genes happen to be active so far anteriorly is because selection has been relaxed, probably because they’ve lost that morphological effect of shutting down ribs. Those big bars are a consequence of simple sloppiness in a system that can afford a little slack.

The next group of Hox genes, the 11 group, are very similar in their expression patterns in the lizard and the snake, and that reflects their specific roles. The 10 group is largely involved in repression of rib formation, but the 11 group is involved in the development of sacrum-specific structures. In birds, for instance, the Hox 11 genes are known to be involved in the development of the cloaca, a structure shared between birds, snakes, and lizards, so perhaps it isn’t surprising that they aren’t subject to quite as much change.

The 13 group has some notable differences: Hox a13 and d13 are mostly shut off in the snake. This is suggestive. The 13 group of Hox genes are the last genes, at the very end of the animal, and one of their proposed functions is to act as a terminator of patterning — turning on the Hox 13 genes starts the process of shutting down the mesoderm, shrinking the pool of tissue available for making body parts, so removing a repressor of mesoderm may promote longer periods of growth, allowing the snake to extend its length further during embryonic development.

So we see a couple of clear correlates at the molecular level for differences in snake and lizard morphology: rib suppression has been lost in the snake Hox 10 group, and the activity of the snake Hox 13 group has been greatly curtailed, which may be part of the process of enabling greater elongation. What are the similarities between snakes and lizards that are also different from other animals?

This was an interesting surprise. There are some differences in Hox gene organization in the squamates as a whole, shared with both snakes and lizards.

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Genomic organization of the posterior HoxD cluster. Schematic representation of the posterior HoxD cluster (from Evx2 to Hoxd10) in various vertebrate species. A currently accepted phylogenetic tree is shown on the left. The correct relative sizes of predicted exons (black boxes), introns (white or coloured boxes) and intergenic regions (horizontal thick lines) permit direct comparisons (right). Gene names are shown above each box. Colours indicate either a 1.5-fold to 2.0-fold (blue) or a more than 2.0-fold (red) increase in the size of intronic (coloured boxes) or intergenic (coloured lines) regions, in comparison with the chicken reference. Major CNEs are represented by green vertical lines: light green, CNEs conserved in both mammals and sauropsids; dark green, CNEs lost in the corn snake. Gaps in the genomic sequences are indicated by dotted lines. Transposable elements are indicated with asterisks of different colours (blue for DNA transposons; red for retrotransposons).

That’s a diagram of the structure of the chromosome in the neighborhood of the Hox d10-13 genes in various vertebrates. For instance, look at the human and the turtle: the layout of our Hox d genes is vary similar, with 13-12-11-10 laid out with approximately the same distances between them, and furthermore, there are conserved non-coding elements, most likely important pieces of regulatory DNA, that are illustrated in light yellow-reen and dark green vertical bars, and they are the same, too.

In other words, the genes that stake out the locations of pelvic and tail structures in turtles and people are pretty much the same, using the same regulatory apparatus. It must be why they both have such pretty butts.

But now compare those same genes with the squamates, geckos, anoles, slow-worms, and corn snakes. The differences are huge: something happened in the ancestor of the squamates that released this region of the genome from some otherwise highly conserved constraints. We don’t know what, but in general regulation of the Hox genes is complex and tightly interknit, and this order of animals acquired some other as yet unidentified patterning mechanism that opened up this region of genome for wider experimentation.

When these regions are compared in animals like turtles and people and chickens, the genomes reveal signs of purifying selection — that is, mutations here tend to be unsuccessful, and lead to death, failure to propagate, etc., other horrible fates that mean tinkering here is largely unfavorable to fecundity (which makes sense: who wants a mutation expressed in their groinal bits?). In the squamates, the evidence in the genome does not witness to intense selection for their particular arrangement, but instead, of relaxed selection — they are generally more tolerant of variations in the Hox gene complex in this area. What was found in those enlarged intergenic regions is a greater invasion of degenerate DNA sequences: lots of additional retrotransposons, like LINES and SINES, which are all junk DNA.

So squamates have more junk in the genomic trunk, which is not necessarily expressed as an obvious phenotypic difference, but still means that they can more flexibly accommodate genetic variations in this particular area. Which means, in turn, that they have the potential to produce more radical experiments in morphology, like making a snake. The change in Hox gene regulation in the squamate ancestor did not immediately produce a limbless snake, instead it was an enabling mutation that opened the door to novel variations that did not compromise viability.

Di-Po N, Montoya-Burgos JI, Miller H, Pourquie O, Milinkovitch MC, Duboule D (2010) Changes in Hox genes’ structure and function during the evolution of the squamate body plan. Nature 464:99-103.

Fodor and Piattelli-Palmarini get everything wrong

People who don’t understand modern evolutionary theory shouldn’t be writing books criticizing evolutionary theory. That sounds like rather pedestrian and obvious advice, but it’s astonishing how often it’s ignored — the entire creationist book publishing industry demands a steady supply of completely clueless authors who think their revulsion at the implications of Darwinian processes is sufficient to compensate for their ignorance. And now Jerry Fodor and Massimo Piattelli-Palmarini, a philosopher and a cognitive scientist, step up to the plate with their contribution to this genre of uninformed folly.

I haven’t read their book, What Darwin Got Wrong, and I don’t plan to; they’ve published a brief summary in New Scientist (a magazine that is evolving into a platform for sensationalistic evolution-deniers, sad to say), and that was enough. It’s breathtaking in its foolishness, and is sufficient to show the two authors are parading about quite nakedly unashamed of their lack of acquaintance with even the most rudimentary basics of modern evolutionary biology.

In our book, we argue in some detail that much the same [they are comparing evolution to Skinner’s behaviorism] is true of Darwin’s treatment of evolution: it overestimates the contribution the environment makes in shaping the phenotype of a species and correspondingly underestimates the effects of endogenous variables. For Darwin, the only thing that organisms contribute to determining how next-generation phenotypes differ from parent-generation phenotypes is random variation. All the non-random variables come from the environment.

Suppose, however, that Darwin got this wrong and various internal factors account for the data. If that is so, there is inevitably less for environmental filtering to do.

I am entirely sympathetic with the argument that naive views of evolution that pretend that populations are infinite plastic and can respond to almost any environmental demand, given enough time, are wrong. I appreciate a good corrective to the excesses of adaptationism; evolution is much more interesting and diverse than the kind of simplistic whetstone it is too often reduced to, but we don’t need bad critiques that veer off into the lunacy of selection-denial. It’s also literally true that Darwin was completely wrong on the basic mechanisms of inheritance operating in organisms — he didn’t know about genes, postulated the existence of distributed information about the organization of tissues and organs that was encapsulated in unobserved mystery blobs called “gemmules” that migrated from the arm, for instance, to the gonads, to pass along instructions on how to build an arm to the gametes. Telling us that Darwin got the chain of information wrong is nothing new or interesting.

It also gets the problem backwards. Darwin’s proposed mechanism actually supported the idea of the inheritance of acquired characters, and as Fodor wants to argue, encouraged the idea that organisms were more responsive to environmental effects than they actually are. The neo-Darwinian synthesis melded the new science of genetics with evolutionary theory, and did make “various internal factors” much more important. They’re called genes.

What do you get when authors who know nothing about genetics and evolution write about genetics and evolution?

This is what makes Fodor and Piattelli-Palmarini’s ideas so embarrassingly bad. They seem to know next to nothing about genetics, and so when they discover something that has been taken for granted by scientists for almost a century, they act surprised and see it as a death-stroke for Darwinism. It’s rather like reading about the saltationist/biometrician wars of the early 1900s, when Mendel was first rediscovered and some people argued that the binary nature of the ‘sports’ described in analyses of inheritance meant the incremental changes described by Darwin were impossible. The ‘problems’ were nonexistent, and were a product merely of our rudimentary understanding of genetics — it was resolved by eventually understanding that most characters of an organism were the product of many genes working together, and that some mutations do cause graded shifts in the phenotype.

Here, for instance, is one of their astonishing revelations about the nature of inheritance:

Darwinists say that evolution is explained by the selection of phenotypic traits by environmental filters. But the effects of endogenous structure can wreak havoc with this theory. Consider the following case: traits t1 and t2 are endogenously linked in such a way that if a creature has one, it has both. Now the core of natural selection is the claim that phenotypic traits are selected for their adaptivity, that is, for their effect on fitness. But it is perfectly possible that one of two linked traits is adaptive but the other isn’t; having one of them affects fitness but having the other one doesn’t. So one is selected for and the other “free-rides” on it.

That is so trivially true that it is a good point to make if you are addressing somebody who is biologically naive, and I think it is a valuable concept to emphasize to the public. But this is Fodor and Piattelli-Palmarini chastising biologists with this awesome fact as if we’ve been neglecting it. It’s baffling. Linkage is a core concept in genetics; Alfred Sturtevant and Thomas Morgan worked it out in about 1913, and it’s still current. The genographic project, which is trying to map out the history of human populations, uses haplotype data — clusters of alleles tend to stay clumped together, only occasionally broken up by recombination, so their arrangements can be used as markers for geneology. The default assumption is that these sets of alleles are not the product of selection, but of chance and history!

They might also look up the concepts of linkage disequilibrium and epistasis. Are we already aware of “free-riding,” background effects, and interactions between genes? Yes, we are. Do we think every trait in every individual is the product of specific selection? You might be able to find a few weird outliers who insist that they are, and perhaps more who regard that as a reasonable default assumption to begin an analysis, but no, it’s obvious that it can’t be true.

It also should be obvious that a fact of genetics that has been known for almost a century and that was part of the neo-Darwinian synthesis from the very beginning isn’t going to suddenly become a disproof of the synthesis when belatedly noticed by a philosopher and neuroscientist in the 21st century.

This time it’s personal: abusing evo-devo

As bad as building an argument on the faulty premise of ignorance might be, there’s another approach that Fodor and Piattelli-Palmarini take that is increasingly common, and personally annoying: the use of a growing synthesis of evolutionary ideas with developmental biology to claim that evolution is dead. This is rather like noting that the replacement of carburetors with electronic fuel injection systems means that internal combustion engines are about to be extinct — evo-devo is a refinement of certain aspects of biology that has, we think, significant implications for evolution, especially of multicellular organisms. It is not a new engine. People who claim it is understand neither development nor evolution.

Fodor and Piattelli-Palmarini throw around a few buzzwords that tell me right away where they’re coming from: they’re jumping on that strange structuralist bandwagon, the one that shows some virtue when the likes of Brian Goodwin are arguing for it, but is also prone to appealing to crackpots like Pivar and Fleury and the ridiculous Suzan Mazur…and now, Fodor and Piattelli-Palmarini.

The consensus view among neo-Darwinians continues to be that evolution is random variation plus structured environmental filtering, but it seems the consensus may be shifting. In our book we review a large and varied selection of non-environmental constraints on trait transmission. They include constraints imposed “from below” by physics and chemistry, that is, from molecular interactions upwards, through genes, chromosomes, cells, tissues and organisms. And constraints imposed “from above” by universal principles of phenotypic form and self-organisation — that is, through the minimum energy expenditure, shortest paths, optimal packing and so on, down to the morphology and structure of organisms.

It’s a shame, too, because there really is some beautiful work done by the structuralist pioneers — this is a field that combines art and mathematics, and has some truly elegant theoretical perspectives. I read the paragraph above and knew instantly what they are referring to — the work of D’Arcy Wentworth Thompson. This D’Arcy Wentworth Thompson:

For the harmony of the world is made manifest in Form and Number, and the heart and soul and all the poetry of Natural Philosophy are embodied in the concept of mathematical beauty.

Ah, but I love Thompson. He wrote the best developmental biology book ever, On Growth and Form, the one that will make you think the most if you can get past the flowery prose (or better yet, enjoy the flowery prose) and avoid throwing it against the wall with great force. It’s another hundred-year-old (almost) book, you see, and Thompson never quite grasped the idea of genes.

The summary I read doesn’t mention the name Thompson even once, but I can see him standing tall in the concepts Fodor is crowing over. My inference was confirmed in a review by Mary Midgley (who, it has rumored, has actually written some sensible philosophy…but every time I’ve read her remarks on biology, comes across as a notable pinhead).

Besides this — perhaps even more interestingly — the laws of physics and chemistry themselves take a hand in the developmental process. Matter itself behaves in characteristic ways which are distinctly non-random. Many natural patterns, such as the arrangement of buds on a stem, accord with the series of Fibonacci numbers, and Fibonacci spirals are also observed in spiral nebulae. There are, moreover, no flying pigs, on account of the way in which bones arrange themselves. I am pleased to see that Fodor and Piattelli Palmarini introduce these facts in a chapter headed “The Return of the Laws of Form” and connect them with the names of D’Arcy Thompson, Conrad Waddington and Ilya Prigogine. Though they don’t actually mention Goethe, that reference still rightly picks up an important, genuinely scientific strand of investigation which was for some time oddly eclipsed by neo-Darwinist fascination with the drama of randomness and the illusory seductions of simplicity.

Her whole review is like that; she clearly adores the fact that those biologists are getting taken down a peg or two, and thinks it delightful that poor long-dead Thompson is the stiletto used to take them out. I’ve got a few words for these clowns posturing on the evo-devo stage.

D’Arcy Wentworth Thompson was wrong.

Elegantly wrong, but still wrong. He just never grasped how much of genetics explained the mathematical beauty of biology, and it’s a real shame — if he were alive today, I’m sure he’d be busily applying network theory to genetic interactions.

Let’s consider that Fibonacci sequence much beloved by poseurs. It’s beautiful, it is so simple, it appears over and over again in nature, surely it must reflect some intrinsic, fundamentally mathematical ideal inherent in the universe, some wonderful cosmic law — it appears in the spiral of a nautilus shell as well as the distribution of seeds in the head of a sunflower, so it must be magic. Nope. In biology, it’s all genes and cellular interactions, explained perfectly well by the reductionism Midgley deplores.

The Fibonacci sequence (1, 1, 2, 3, 5, 8…each term generated by summing the previous two terms) has long had this kind of semi-mystical aura about it. It’s related to the Golden Ratio, phi, of 1.6180339887… because, as you divide each term by the previous term, the ratio tends towards the Golden Ratio as you carry the sequence out farther and farther. It also provides a neat way to generate logarithmic spirals, as we seen in sunflowers and nautiluses. And that’s where the genes sneak in.

There’s an easy way to generate a Fibonacci sequence graphically, using the method of whirling squares. Look at this diagram:

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Start with a single square on a piece of graph paper. Working counterclockwise in this example, draw a second square with sides of the same length next to it. Then a third square with the same dimensions on one side as the previous two squares. Then a fourth next to the previous squares…you get the idea. You can do this until you fill up the whole sheet of paper. Now look at the lengths of each side of the squares in the series — it’s the Fibonacci sequence, no surprise at all there.

You can also connect the corners with a smooth curve, and what emerges is a very pretty spiral — like a nautilus shell.

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It’s magic! Or, it’s mathematics, which sometimes seems like magic! But it’s also simple biology. I look at the whirling squares with the eyes of a developmental biologist, and what do I see? A simple sequential pattern of induction. A patch of cells uses molecules to signal an adjacent patch of cells to differentiate into a structure, and then together they induce a larger adjacent patch, and together they induce an even larger patch…the pattern is a consequence of a mathematical property of a series expressed on a 2-dimensional sheet, but the actual explanation for why it recurs in nature is because it’s what happens when patches of cells recruit adjacent cells in a temporal sequence. Abstract math won’t tell you the details of how it happens; for that, you need to ask what are the signaling molecules and what are the responding genes in the sunflower or the mollusc. That’s where Thompson and these new wankers of the pluralist wedge fail — they stop at the cool pictures and the mathematical formulae and regard the mechanics of implementation as non-essential details, when it’s precisely those molecular details that generate the emergent property that dazzles them.

Let’s consider another classic Thompson example. Thompson was well-known for his work on how different forms could be generated by allometric transformations, and here’s one of his illustrations showing the relationship between the shape of the pelvis in Archaeopteryx and Apatornis, a Cretaceous bird. He’s making the point that one seems to be a relatively simple geometric transformation of the other, that you could describe one in terms of the changes in a coordinate grid.

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By use of simple mathematical transforms, one can generate a whole range of intermediates, fitting perfectly with the Darwinian idea of incremental change over time. Again, this is where Thompson falls short; he’s so enamored with the ideal of a mathematical order that he doesn’t consider the implementation of the algorithm in real biology.

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That mechanism of making the transformation is the crucial step. Thompson can see it as a distortion of a coordinate grid, but there is no grid in the organism. What there are are populations of cells in the developing embryo that interact with each other through molecular signals and changes in gene expression; the form is the product of an internal network of genes regulating each other, not an external ideal. Ignore the artificial grid, and imagine instead a skein of genes in a complex regulatory network, changes in one gene propagating as changes in the pattern of expression of other genes. A mutation in one gene tugs on the whole skein, changing the outcome of development in a way that is, by the nature of the whole complex, going to involve shifts in the pattern of the whole regulated structure.

There is nothing in this concept that vitiates our modern understanding of evolutionary theory, the whole program of studying changes in genes and their propagation through populations. That’s the mechanism of evolutionary change. What evo-devo does is add another dimension to the issue: how does a mutation in one gene generate a ripple of alterations in the pattern of expression of other genes? How does a change in a sequence of DNA get translated into a change in form and physiology?

Those are interesting and important questions, and of course they have consequences on evolutionary outcomes…but they don’t argue against genetics, population genetics, speciation theory, mutation, selection, drift, or the whole danged edifice of modern evolutionary biology. To argue otherwise is like claiming the prettiness of a flower is evidence against the existence of a root.

We’re all pluralists now

We’re just not all willing to admit it, and some of us tend to overemphasize our own disciplines too much. I admit that I think the most interesting, key innovations in metazoan evolution all involve shifts in gene regulation — recombinations of genes, novel interactions between genes being more important than new genes themselves. Others will argue that those are changes in genes, and that focusing on regulation is not so much a dramatic revolution as a narrowing of interest to a subset of heritable change. I will say that evolutionary history is dominated by random chance, that all those “free-riders” that Fodor and Piattelli-Palmarini sieze upon as arguments against evolution are actually the coolest aspects of evolution, and represent the bulk of the diversity and specializations that we see in the natural world. Others will argue that selection is the engine of functionality, the one process that produces useful adaptations.

We’re all arguing for the same core ideas, though, just emphasizing different aspects. Life on earth evolved. Selection is the process that produces more efficient matching of organism to the environment, chance is the process that produces greater diversity. We all study these processes through our own lenses, our own specialties, and complaining that Charles Darwin’s lens had defects is irrelevant and silly — we already knew that, just as we all know our own lenses are imperfect. That’s why we all work together and argue and argue and argue, testing our ideas, trying to work out clearer, closer approximations to the truth.

Fodor and Piattelli-Palmarini are following on a grand tradition of noticing the fact that evolution is complex and uses a multiplicity of mechanisms to play one strand of science against another; that because one discipline emphasizes selection and another emphasizes diversity and another emphasizes regulation and another emphasizes coding sequences, the differences between each mean the whole tapestry must be wrong. It’s fallacious reasoning. (I must also add that arguing that just one strand is the important one is also the wrong way to address the problem.) All it demonstrates is that they are blind to the big picture of evolutionary biology.

It’s also embarrassing to a developmental biologist that they should try to ride our field as if it were a refutation of that big picture of evolutionary biology. They can talk about constraints and gene regulatory networks and developmental mechanics all they want, but don’t be fooled: neither Fodor nor Piattelli-Palmarini are developmental biologists. Their authority is that of the bystanding dilettante, and while they mouth the words, they don’t seem to grasp the meaning.