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.

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.

I’m a starry-eyed techno-utopian, and proud of it

Freeman Dyson (with whom I have many disagreements, so don’t take this as an unqualified endorsement), wrote an interesting article that predicted, in part, a coming new age of biology. I think he’s entirely right in that, and that we can expect amazing information and changes in this next century.

If the dominant science in the new Age of Wonder is biology, then the dominant art form should be the design of genomes to create new varieties of animals and plants. This art form, using the new biotechnology creatively to enhance the ancient skills of plant and animal breeders, is still struggling to be born. It must struggle against cultural barriers as well as technical difficulties, against the myth of Frankenstein as well as the reality of genetic defects and deformities.

Apparently, this freaks some people out. The so-called Crunchy Con, a knee-jerk Catholic nicely described as a “weird, humorless, smart, spooky, self-rightous, puritan wingnut”, is one of the people who takes particular exception to this optimistic view of the future. Rod Dreher wrote an egregiously ignorant whine about the possibilities, which I will proceed to puke upon.

[Read more…]

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.

Crawling pigments

Here’s another of Casey Dunn’s Creature Casts, this time on shifting color spots in marine snails.

CreatureCast – Flamingo Tongue Snails from Casey Dunn on Vimeo.

Pigment cells are always very, very cool. I’ve been intrigued by them for a long time — they show up in my time-lapse recordings of developing zebrafish and are always active. Here’s a quick one, a few hours of time in a roughly 24 hour old zebrafish embryo, compressed to about 30 seconds. You can see one corner of the dark eye at the bottom left of the image, and that oval structure near the middle with two spots in it is the ear and its otoliths. The melanocytes are writhing over the side of the head and down onto the yolk sac; they’re not quite as colorful as the snail, but then, the zebrafish is a mostly black and white animal.

Evo-devo on NOVA

Don’t miss it! Tonight at 8pmET/7pm Central, NOVA is showing What Darwin Never Knew, a documentary about evo-devo. I shall be glued to my TV tonight!

I just started watching it. So far, it’s a nice little history of Darwin and his ideas; Sean Carroll is a good person to have talking up the story. It’s nothing new yet, and nothing about evo-devo so far — I’m waiting impatiently for it.

Twenty minutes in, we get a little embryology: limb rudiments in snake embryos, tooth rudiments in whale embryos, and branchial arches in human embryos. These are shown as uncompromising evidence of limbed, toothed, and gilled ancestors — cue wails of horror from the Discovery Institute…now.

They also discuss variation in dog breeds. More development, please!

Hmmm. We’re past the half-hour mark, and it’s all selection, selection, selection. It’s clearly explained and it’s a useful intro to the general concept of Darwinian evolution…but I was hoping for something a little more focused and novel. This documentary is supposed to be based on Carroll’s Endless Forms Most Beautiful and The Making of the Fittest, but we’re getting bogged down in very general material and not yet getting to the meat of either book.

Now we’re getting an explanation of DNA sequences as a code (alarms are whooping at the Discovery Institute again), with pigment changes in different varieties of mice as an example. We’re also getting brief mentions of genetic changes that produce color vision and cold-adaptedness in icefish (those are straight from Making of the Fittest).

This bugs me. They’re talking about the number of genes in the human genome as a big surprise — we “only” have 23,000 genes. I don’t know; it always seems to be dropped out of context. How many genes should we have expected?

Some nice animations of transformations of embryos are shown, illustrating (as Haeckel did) that all vertebrates began with a common body plan that diverges in detail over the course of development — I hope an ambulance is on standby in Seattle near the DI.

Unfortunately, they’re using developmental changes as an explanation for why we have too few genes to satisfy our egos. Again, this bugs me: fruit flies and people have comparable numbers of genes, and also comparable developmental processes.

Anyway, it does lead into some useful discussion of evolving pigmentation spots in Drosophila, which leads further into regulatory DNA. Unfortunately, this bit has some confusing stuff. The documentary conflates regulatory DNA with junk DNA — regulatory is not and has not been regarded as junk! — and might lead some viewers into thinking that all junk DNA has developmental functions. It does not.

They do have some nice illustrations of experiments used to tag regulatory sequences with marker genes, making flies with glowing spots on their wings.

Another good example: they’re showing the evolution of regulatory switches in stickleback fish. Cool, it’s David Kingsley! They’re showing how the differences between marine (spiky) and freshwater (non-spiky) is not in the coding sequences of a few genes, but in the regulatory regions of those genes.

Hmm. Repetitive flashy graphics of DNA are beginning to hurt my eyes.

We also get a summary of Tabin’s work on the genes behind different beak morphologies in finches. The same genes are involved, but the differences are in the timing and strength of activation of these genes. The genes involved are also explained as regulatory genes — the genes that switch other genes off and on. This is starting to get into stuff I’d find useful in the classroom.

Hey, now it’s Neil Shubin’s turn to talk about the evolution of limbs. This show is turning out to be a nice introduction to the superstars of evo-devo!

More cool stuff: video from Ellesmere Island, and the discovery of Tiktaalik. Also an amusing animation of the fossil coming to life in Shubin’s lab, which I’m pretty sure doesn’t actually happen.

The show quickly moves from fossils to molecules, and describes efforts to isolate the limb regulatory pathway from modern relatives (paddlefish) of the ancient tetrapods. We get to hear a little bit about Hox genes. Oooh, I could use some of those sequences illustrating the pattern of Hox gene expression in the limb…

We don’t need new genes to make new structures: changing the timing and strength of expression of genes within an existing pathway can create new features.

At least, a clear statement of what Darwin didn’t know that the documentary is describing: we are deriving mechanistic explanations for the processes that produce morphological diversity. It’s a consequence of subtle shifts in the timing and intensity of gene expression in a hierarchy of well-established functional pathways.

We’re getting into the last half-hour here, and the emphasis is switching to humans. Ho-hum. Humans are really crummy experimental models, so I guess we’re not going to get deeper into those mechanisms, but will tap into the audience’s self-centeredness, which they need to do, I guess.

At least they’re focusing a bit: they promise to tell us about the genetics of hand development, and specifically of the thumb. They’re scanning genes that are different between humans and chimpanzees, looking for molecules that suggest they play a role in the differences in digits. A gene is found that is active in the thumb and big toe, and also differs significantly in sequence between us and the chimps. This is work I’m unfamiliar with — it would be nice if they named the gene for us!

Noooo…we’re teased with some interesting work, and now it’s flitting off to talk about the brain.

Another tease: a researcher identifies a gene that differs between humans and chimpanzees, and is defective in humans; it’s involved in chewing muscles. It is suggested that knocking out this gene was part of the process of freeing up the expansion of the cranium. It’s a frustrating part of the medium that it makes it hard to dig up more specific citations. (OK, here’s a short article on Stedman’s work).

They do it again with a regulator of neuronal growth involved in microcephaly: name the gene, please. They keep talking around it, calling it “this gene” or “the key gene”. It’s just odd that they ignore one of the conventions of molecular biology, failing to give us a name that we can use as a handle. It’s going to make it difficult to talk about over the water cooler tomorrow, isn’t it?

Olivia Judson relates it all back to Darwin: he was the beginning, not the end of evolutionary biology.

My opinion overall: the first half hour was boring to me — it was an extremely basic primer in old-school Darwinian biology. The middle hour was of more interest, and did get into real evolutionary developmental biology, and showed off some of the best examples of work in the field. This was the bit I’d find most useful in my classes; that first half-hour was too basic for most freshman biology majors.

I wasn’t too keen on the last bit where it got very human-centric, but I can see where the examples they talked about would provoke viewer interest. I just wish it were possible for the medium to push a little deeper into the topics than they did.

Carroll, Shubin, and Tabin were good. Make them TV stars!

Get your geek on for Thursday

I’m going to be opening my mouth again on Thursday in Minneapolis — I’ll be giving a talk in MCB 3-120 on the Minneapolis campus at 7:30 on Thursday, 3 December. This will be open to the public, and it will also be an all-science talk, geared for a general audience. I’d say they were going to check your nerd credentials at the door, but just showing up means you’re already fully qualified.

The subject of the talk is my 3 big interests: a) evolution, or how we got here over multiple generations, b) development, or how we got here in a single generation, and c) the nervous system, the most complicated tissue we have. I intend to give a rough outline of how nervous tissue works, how it is assembled into a working brain, and how something so elaborate could have evolved. All in one hour. Wheee!

Afterwards, we’ll be joining the CASH gang for refreshments, somewhere. They haven’t told me yet where, but I know they’re fond of pizza.

IGERT2009: Sunday morning session

My little laptop is functional again, so at least I’ll be able to blog these Sunday morning IGERT sessions in real-time. I still have to transcribe my notes from yesterday; I’ll plan on getting that done on the plane this afternoon.

Kristi Montooth: Mitochondrial-nuclear epistasis for metabolic fitness in flies

How do physiological systems evolve to maintain metabolic fitness? This is a process that involves interactions between two genomes, the nuclear and mitochondrial. Energy metabolism is important and is the target of mutation, but the same players are found all across the tree of life, suggesting that there is also strong selective pressure to maintain a common system.

Montooth is looking at inducible gene expression: is there an energetic cost to switch genes off and on? She’s using respirometers that can measure the metabolic rate of single flies or larva. Flies are subjected to heat shock, which switches on HSP70. Flies normally have 6 copies of HSP70; they have mutants with 12, and they show a much greater rise in metabolic rate in response to heat shock.

Mitochondria are the source of the energy for this response. Mitochondria also have a high mutation rate and show strong linkage (no sexual recombination to cover for errors that arise). She’s arguing for selection for compensatory evolution in the nuclear genome, and the accumulation of intergenomic epistasis. To dissect the effects of coevolution of mitochondria and nuclear genomes, she transplanted mitochondria from different species into Drosophila melanogaster. These have between 18 and 100 amino acid substitutions from the Dmel sequence.

She plots mitochondrial genome in order of increasing divergence against measured fitness (she used a competition assay that she did not describe in detail). There is no correlation seen at all. Also, high fitness X/mtDNA genotypes in one sex can be low fitness genotypes in the other sex. Interactions between the X and mtDNA can maintain variation in both genomes. All of the fitness effects, with one exception, are subtle.

Some of the transgenomic effects have very strong effects on female fecundity, developmental rates, and locomotion. But adult metabolic rate shows no difference! The idea is that there are lots of homeostatic mechanisms that maintain metabolism very tightly, which then have secondary effects.

Johanna Schmitt: Adaptive evolution of Arabidopsis flowering pathways in different climates

Schmitt does ecological development, looking at the timing of plant development in different environments. How does phenology respond and adapt to climate variation? We expect evolution to adapt to variation in seasonal timing. The signaling pathways in Arabidopsis are well known; they respond to hormones, photoperiod, and ambient temperature by way of a fairly complicated set of pathways she showed us in a slide…sorry, no way I can reproduce it here!

Across its range, it shows a great deal of life history variation; one pattern in the Mediterranean, another in colder northern climes, and yet another in Northern Scandinavia, varying in how much time they spend in vegetative rosettes vs. bolting and flower production. Questions: are there are genetic variants associated with different life history patterns, can they identify the genes, and can they perturb them?

The experiments involved massive plantings in different sites in Europe with different climates, with different mutants. Is natural variation in candidate genes involved in variation in flowering time? They studied FRIGIDA, a gene that effects the vernalization pathway. When you lose FRIGIDA, you should see much more rapid flowering. Loss of function in this gene has evolved multiple times in northwestern Europe. The effect depends on the timing of planting and climate.

The effect of the mutant varies across geography, and they have a photothermal model of flowering time. The plants are tracking light and temperature, and the different mutants are counting up these inputs in slightly different ways. They can use this model to make predictions on the effects of FRIGIDA on flowering time with changes in germination timing, and then test these in the next year with plantings at different times and in their different geographical sites, and the model is working accurately.

They are also plugging in predicted future climate change from NOAA, and asking what we can expect to see 100 years from now; she showed maps of expected flowering times in 2100. They are also making predictions of the expected distributions of FRIGIDA alleles over time, and they hope to do the same for many other alleles in Arabidopsis.

Artyom Kopp: How the fly got its sexy legs – the origin and evolution of Drosophila sex combs

The sex comb is a male specific structure on the front legs which most Drosophila species lack — it’s a fairly recent innovation. How do you evolve a novel structure?

It’s limited to the melanogaster and obscura species groups, with quite a bit of diversity in different species, varying from 2-50 teeth, location, and arrangement. How do you go from sexually monomorphic state of a generically hairy leg to one with a specific bristle arrangement in males? The sex comb in males is homologous to a subset of bristles also found in females; in males, that patch of epidermis rotates 90° and the bristles enlarge. He showed a very pretty developmental series of this epithelium undergoing cell shape changes that move the bristles to a new location. Other species show similar morphological remodeling, but sometimes with some significant differences: D. kikkawai doesn’t do the rotation, but instead the bristle precursors arise in their final position. These modes do not cluster together phylogenetically, so these are examples of convergent evolution, generating similar structures with different mechanisms.

They are taking apart the genetics and regulatory inputs of sex comb development. Basically, it involves just about everything. It seems to arise by an interaction between Hox and sex determination genes. Spatial modulation of Sex combs reduced controls sex comb position. Scr in pupa; stages is only expressed in a limited domain in the leg, and ectopic expression of Scr produces multiple sex combs. Expression is also sexually dimorphic, with no upregulation of Scr in female legs. In D. ficusphila, which has enormous sex combs, Scr levels are elevated yet further to 7 times the levels found in D. willistoni.

The sex determination gene Double sex is also spatially patterned, and is refined and elevated to high levels in the area around the developing sex combs. Ectopic expression of Dsx induces ectopic sex combs.

How can a new developmental pathway evolve? In the ancestral condition, Scr is controlled by spatial cues to produce segmental patterns of bristles; in the sex-comb carrying species, Scr is coupled to Dsx. This explains the spatial pattern of gene expression, but it also needs to acquire new downstream targets to, for instance, regulate epidermal rotations.

Drosophila are old, and many of these species differences are millions of years old. They are now looking at more recently diverged species with differences in sex comb morphology, and are looking for correlations between Scr and species divergence.

And with that, I have to run for the airport shuttle. Good talks, and I unfortunately have to miss Rudy Raff’s wrap-up of the meeting.

A creationist at the Chicago meeting

Last week, I described the lectures I attended at the Chicago 2009 Darwin meetings (Science Life also blogged the event). Two of the talks that were highlights of the meeting for me were the discussions of stickleback evolution by David Kingsley and oldfield mouse evolution by Hopi Hoekstra — seriously, if I were half my age right now, I’d be knocking on their doors, asking if they had room for a grad student or post-doc or bottle-washer. They are using modern techniques in genetics and molecular biology to look at variation in natural populations in the wild, and working out the precise genetic changes that led to the evolution of differences in development and morphology. They are doing stuff that, back when I actually was a graduate student, would have been regarded as technically impossible; you needed model systems in the laboratory to have the depth of molecular information required to track down the molecular basis of novel morphs, and you couldn’t possibly just grab some interesting but otherwise unknown species out on a beach or a pond and work out a map and localize genetic differences between individuals. They’re doing it now, though, and making it look easy.

Then there were all the other talks in population genetics and paleontology (and the talks on history and philosophy, which I almost entirely neglected)…this was a meeting that everywhere demonstrated major advances in our understanding of evolution. Every talk was about the successes of evolutionary theory and directions to take to overcome incomplete areas of understanding; this was a wonderfully positive and promising event that should have impressed all the attendees with the quality of the work that has been done and the excitement of the potential for future research. Like I said, there were a whole bunch of people here that I want to be when I grow up.

Well, normal people would feel that way. Paul Nelson, that creationist, was also there. Nelson is a weird guy; he’s always hanging around the edges of these scientific meetings, and you’d think that after all these years of lurking, he’d actually learn something, but no…the only skill he has mastered is the art of ignoring what he doesn’t like and incorporating fragments of sentences into his armor of ignorance. It’s very sad.

I talked with Nelson briefly at a reception at the meetings, and we both agreed on the quality of Kingsley’s work — but that’s about all. Nelson thought it supported ID better than neo-Darwinian evolutionary theory. His argument was that a) all anybody ever described was loss of features, and b) a large parent population was the source of all the allelic variation in the sub-populations studied, which is what ID predicts. He didn’t mention their favorite magic word of “front-loading”, but I could see what he was thinking.

How Nelson can hang about on the fringes of the evo-devo world and not notice that what was described by modern empirical research is exactly what the evo-devo theoreticians expected is a mystery — these were results that fit beautifully what science, not the wishful voodoo of intelligent design creationism, predicts.

Both Kingsley and Hoekstra are looking at recent species, subpopulations that separated from parent populations within the last ten thousand years, and have adapted relatively rapidly to new environmental conditions. The sticklebacks are fragments of marine species that were isolated in freshwater streams and lakes, while the beach mice are parts of a widespread population of oldfield mice that are adapting to gulf coast islands. They are also working with populations that can be bred back to the root stock, that retain the ability to do genetic crosses, so of course the variation is not on the magnitude of turning fins into limbs (we need large amounts of geological time to do that; it’s the kind of work Neil Shubin would do, and unfortunately, he can’t cross Tiktaalik with Acanthostega). Complaining that the variants the real scientists are looking at aren’t the kind that the creationists want is a particularly clueless kind of whine, since the scientists are intentionally focusing on the variants that are amenable to dissection by their techniques.

The other aspect of their work that confirms evo-devo expectations is that what they’re discovering is that the genetic mechanisms behind morphological variants are changes in regulatory DNA — that what’s happening is that regulatory genes like Pitx1 or Mc1r are being switched off or on. We anticipate that a lot of morphological novelty is going to be generated by switching genes off and on, and by recombination of patterns of gene expression. Nelson and Behe are reduced to carping on the sidelines that observed variants are just the product of getting large effects by trivially flipping switches, while all the real biologists are out there in the middle of the work happily announcing that we can get large-scale morphological effects by simply flipping switches, and hey, isn’t that cool, and doesn’t that tell us a lot about the origins of evolutionary novelties? It’s not just a to-may-to/to-mah-to difference in interpretation, this is a case of the creationists wilfully and ignorantly missing the whole point of an exciting line of research.

There’s also a fundamental failure of comprehension. Creationists see loss of a feature like pelvic spines, or a reduction in pigmentation, and declare that the evolutionary evidence is “all breaking things and losing things”. Wrong. What we have here is a complete lack of understanding of developmental genetics. What we typically find are changes in the pattern of expression of developmental genes, not wholesale losses. In the stickleback, Pitx1 is still there; what’s different is that the places in the embryo where it is turned on have changed, the map of the pattern of gene expression has shifted. You cannot describe that as simply a broken gene. Similarly, in the mouse, Hoekstra showed that the expression of genes that reduce pigmentation has expanded. We’ve seen the same thing in the blind cavefish; a creationist looks at it and says it’s just broken and has lost its eyes, but the scientists look closer and see that no, the fish have actually increased gene expression and expanded the domain of a midline gene.

Just wait for the detailed analysis of jaw morphology in cichlid fishes. These animals have radically different variants in feeding structures, which is thought to be the root of their adaptability and the radiation of different forms, and I guarantee you that the creationists will ignore the morphological novelties and focus on the fact that to achieve that, some genes will be downregulated (I also guarantee you that there will be such shifts in expression). It’s “all breaking things and losing things”, after all; just like baking a cake involves breaking eggs.

I don’t know how the creationists fit known variations in the coding sequences of genes (how do you translate a single-nucleotide polymorphism into their vision of all change being a matter of losses?) into their idea that all evolution is a matter of breaking DNA, or how they can claim all novelty requires a designer when people can track the progression of morphological shifts in the tetrapod transition, for instance, across tens of millions of years. It seems to be their desperate 21st century excuse in the face of the overwhelming progression of information from 21st century biological science.

Nelson ends his skewed summary of the meeting with the comment that “It’s a heck of a lot of fun to attend a conference like this, if you don’t mind being the butt of jokes.” I’m sure. I suppose Nelson could have even more fun if he put on a dunce cap and drooled a lot, because that’s basically his role at these meetings anyway — he’s the butt of jokes because he shows up and then happily demonstrates his ignorance about what’s going on. It’s not a role I’d enjoy, but the gang at the clown college called the Discovery Institute have a slightly different perspective, I suppose.