Here’s part of an explanation I’ve liked for a long time: they’re a product of developing cognitive processes that bias the brain to model the world with supernatural shortcuts.
(Moved below the fold because the silly video defaults to autoplay.)
I’m liking these CreatureCast videos from Casey Dunn — I showed the first in this series, now here’s the second. It uses very simple animation to illustrate basic concepts…like the evolution of multicellularity in this one.
CreatureCast Episode 2 from Casey Dunn on Vimeo.
I was just catching up on a few blogs, and noticed all this stuff I missed about Jonathan Wells’ visit to Oklahoma. And then I read Wells’ version of the event, and just about choked on my sweet mint tea.
The next person–apparently a professor of developmental biology–objected that the film ignored facts showing the unity of life, especially the universality of the genetic code, the remarkable similarity of about 500 housekeeping genes in all living things, the role of HOX genes in building animal body plans, and the similarity of HOX genes in all animal phyla, including sponges. 1Steve began by pointing out that the genetic code is not universal, but the questioner loudly complained that 2he was not answering her questions. I stepped up and pointed out that housekeeping genes are similar in all living things because without them life is not possible. I acknowledged that HOX gene mutations can be quite dramatic (causing a fly to sprout legs from its head in place of antennae, for example), but 3HOX genes become active midway through development, 4long after the body plan is already established. 5They are also remarkably non-specific; for example, if a fly lacks a particular HOX gene and a comparable mouse HOX gene is inserted in its place, the fly develops normal fly parts, not mouse parts. Furthermore, 6the similarity of HOX genes in so many animal phyla is actually a problem for neo-Darwinism: 7If evolutionary changes in body plans are due to changes in genes, and flies have HOX genes similar to those in a horse, why is a fly not a horse? Finally, 8the presence of HOX genes in sponges (which, everyone agrees, appeared in the pre-Cambrian) still leaves unanswered the question of how such complex specified genes evolved in the first place.
The questioner became agitated and shouted out something to the effect that HOX gene duplication explained the increase in information needed for the diversification of animal body plans. 9I replied that duplicating a gene doesn’t increase information content any more than photocopying a paper increases its information content. She obviously wanted to continue the argument, but the moderator took the microphone to someone else.
It blows my mind, man, it blows my freakin’ mind. How can this guy really be this stupid? He has a Ph.D. from UC Berkeley in developmental biology, and he either really doesn’t understand basic ideas in the field, or he’s maliciously misrepresenting them…he’s lying to the audience. He’s describing how he so adroitly fielded questions from the audience, including this one from a professor of developmental biology, who was no doubt agitated by the fact that Wells was feeding the audience steaming balls of rancid horseshit. I can’t blame her. That was an awesomely dishonest/ignorant performance, and Wells is proud of himself. People should be angry at that fraud.
I’ve just pulled out this small, two-paragraph fragment from his longer post, because it’s about all I can bear. I’ve flagged a few things that I’ll explain — the Meyer/Wells tag team really is a pair of smug incompetents.
1The genetic code is universal, and is one of the pieces of evidence for common descent. There are a few variants in the natural world, but they are the exceptions that prove the rule: they are slightly modified versions of the original code that are derived by evolutionary processes. For instance, we can find examples of stop codons in mitochondria that have acquired an amino acid translation. You can read more about natural variation in the genetic code here.
2That’s right, he wasn’t answering her questions. Meyer was apparently bidding for time until the big fat liar next to him could get up a good head of steam.
3This implication that Hox gene expression is irrelevant because it is “late” was a staple of Wells’ book, Icons of Evolution and the Politically Incorrect Guide to Darwinism and Intelligent Design. It’s a sham. The phylotypic stage, when the Hox genes are exhibiting their standard patterns of expression, of humans is at 4-5 weeks (out of 40 weeks), and in zebrafish it’s at 18-24 hours. These are relatively early events. The major landmarks before this period are gastrulation, when major tissue layers are established, and neurulation, when the neural tube forms. Embryos are like elongate slugs with the beginnings of a few tissues before this time.
4What? Patterned Hox gene expression is associated with the establishment of the body plan. Prior to this time, all the embryonic chordate has of a body plan is a couple of specified axes, a notochord, and a dorsal nerve tube. The pharyngula stage/phylotypic stage is the time when Hox gene expression is ordered and active, when organogenesis is ongoing, and when the hallmarks of chordate embryology, like segmental myotomes, a tailbud, and branchial arches are forming.
5Hox genes are not non-specific. They have very specific patterning roles; you can’t substitute abdominal-B for labial, for instance. They can be artificially swapped between individuals of different phyla and still function, which ought, to a rational person, be regarded as evidence of common origin, but they definitely do instigate the assembly of different structures in different species, which is not at all surprising. When you put a mouse gene in a fly, you are transplanting one gene out of the many hundreds of developmental genes needed to build an eye; the eye that is assembled is built of 99% fly genes and 1% (and a very early, general 1%) mouse genes. If it did build a mouse eye in a fly, we’d have to throw out a lot of our understanding of molecular genetics and become Intelligent Design creationists.
Hox genes are initiators or selectors; they are not the embryonic structure itself. Think of it this way: the Hox genes just mark a region of the embryo and tell other genes to get to work. It’s as if you are contracting out the building of a house, and you stand before your subcontractors and tell them to build a wall at some particular place. If you’ve got a team of carpenters, they’ll build one kind of wall; masons will build a different kind.
6No, the similarity of Hox genes is not a problem. It’s an indicator of common descent. It’s evidence for evolution.
7Good god.
Why is a fly not a horse? Because Hox genes are not the blueprint, they are not the totality of developmental events that lead to the development of an organism. You might as well complain that the people building a tarpaper shack down by the railroad tracks are using hammers and nails, while the people building a MacMansion on the lakefront are also using hammers and nails, so shouldn’t their buildings come out the same? Somebody who said that would be universally regarded as a clueless moron. Ditto for a supposed developmental biologist who thinks horses and flies should come out the same because they both have Hox genes.
8You can find homeobox-containing genes in plants. All that sequence is is a common motif that has the property of binding DNA at particular nucleotide sequences. What makes for a Hox gene, specifically, is its organization into a regulated cluster. How such genes and gene clusters could arise is simply trivial in principle, although working out the specific historical details of how it happened is more complex and interesting.
The case of sponges is enlightening, because they show us an early step in the formation of the Hox cluster. Current thinking is that sponges don’t actually have a Hox cluster (the first true Hox genes evolved in cnidarians), they have a Hox-like cluster of what are called NK genes. Apparently, grouping a set of transcription factors into a complex isn’t that uncommon in evolution.
9If you photocopy a paper, the paper doesn’t acquire more information. But if you’ve got two identical twins, A who is holding one copy of the paper, and B who is holding two copies of the same paper, B has somewhat more information. Wells’ analogy is a patent red herring.
The ancestral cnidarian proto-Hox cluster is thought to have contained four Hox genes. Humans have 39 Hox genes organized into four clusters. Which taxon contains more information in its Hox clusters? This is a trick question for Wells; people with normal intelligence, like most of you readers, would have no problem recognizing that 39 is a bigger number than 4. Jonathan Wells seems to have missed that day in his first grade arithmetic class.
It’s appalling, but this is the Discovery Institute’s style: to trot out a couple of crackpots with nice degrees, who then proceed to make crap up while pretending to be all sincere and informed and authoritative. It’s an annoying trick, and I can understand entirely why a few intelligent people with actual knowledge in the audience might find the performance infuriating. I do, too.
It’s yet another transitional fossil! Are you tired of them yet?
Darwinopterus modularis is a very pretty fossil of a Jurassic pterosaur, which also reveals some interesting modes of evolution; modes that I daresay are indicative of significant processes in development, although this work is not a developmental study (I wish…having some pterosaur embryos would be exciting). Here it is, one gorgeous animal.
One important general fact you need to understand to grasp the significance of this specimen: Mesozoic flying reptiles are not all alike! There are two broad groups that can be distinguished by some consistent morphological characters.
The pterosaurs are the older of the two groups, appearing in the late Triassic. They tend to have relatively short skulls with several distinct openings, long cervical (neck) ribs, a short metacarpus (like the palm or sole of the foot), a long tail (with some exceptions), and an expanded flight membrane suspended between the hind limbs, called the cruropatagium. They tend to be small to medium-sized.
The pterodactyls are a more derived group that appear in the late Jurassic. Their skulls are long and low, and have a single large opening in front of the eyes, instead of two. Those neck ribs are gone or reduced, they have a long metacarpus and short tails, and they’ve greatly reduced the cruropatagium. Some of the pterodactyls grew to a huge size.
Here’s a snapshot of their distribution in time and phylogenetic relationships. The pterosaurs are in red, and the pterodactyls are in blue.
Darwinopterus is in there, too—it’s the small purple box numbered “7”. You can see from this diagram that it is a pterosaur in a very interesting position, just off the branch that gave rise to the pterodactyls. How it got there is interesting, too: it’s basically a pterosaur body with the head of a pterodactyl. Literally. The authors of this work carried out multiple phylogenetic analyses, and if they left the head out of the data, the computer would spit out the conclusion that this was a pterosaur; if they left the body out and just analyzed the skull, the computer would declare it a pterodactyl.
What does this tell us about evolution in general? That it can be modular. The transitional form between two species isn’t necessarily a simple intermediate between the two in all characters, but may be a mosaic: the anatomy may be a mix of pieces that resemble one species more than the other. In this case, what happened in the evolution of the pterodactyls was that first a pterodactyl-like skull evolved in a pterosaur lineage, and that was successful; later, the proto-pterodactyls added the post-cranial specializations. Not everything happened all at once, but stepwise.
This should be a familiar concept. In pterodactyls, skulls evolved a specialized morphology first, and the body was shaped by evolutionary processes later. We can see a similar principle in operation in the hominid lineage, too, but switched around. We evolved bipedalism first, in species like Ardipithecus and Australopithecus, and the specializations of our skull (to contain that big brain of which we are so proud) came along later.
As I mentioned at the beginning, this is an example of development and evolution in congruence. We do find modularity in developmental process — we have genetic circuits that are expressed in tissue- and region-specific ways in development. We can talk about patterns of gene expression that follow independent programs to build regions of the body, under the control of regional patterning genes like the Hox complex. In that sense, what we see in Darwinopterus is completely unsurprising.
What is interesting, though, is that these modules, which we’re used to seeing within the finer-grained process of development, also retain enough coherence and autonomy to be visible at the level of macroevolutionary change. It caters to my biases that we shouldn’t just pretend that all the details of development are plastic enough to be averaged out, or that the underlying ontogenetic processes will be overwhelmed by the exigencies of environmental factors, like selection. Development matters — it shapes the direction evolution can take.
Lü J, Unwin DM, Jin X, Liu Y, Ji Q (2009) Evidence for modular evolution in a long-tailed pterosaur with a pterodactyloid skull. Proc. R. Soc. B published online 14 October 2009 doi: 10.1098/rspb.2009.1603
I should have mentioned that Darren Naish has a very thorough write-up on Darwinopterus!
Look at the interesting snake found in China — it’s got a leg.
How can this happen? Genes are pleiotropic — they tend to have lots of different functions. The genes involved in making a limb are also expressed in other places; for instance, the Hox genes that specify identity along the length of the body are also reused in specifying identity along the length of the limb. What that means is that when the snake evolved limblessness, it didn’t do so by simply throwing away a collection of leg genes — it couldn’t, not without also destroying genes that functioned in generating its body plan. Instead, it evolved genes or modified the regulation of genes to actively suppress limb development…but the genes to build a limb are still in the genome, and still functional, and still actively working in other ways.
What most likely happened here is that some environmental agent suppressed the suppressor, allowing the old developmental program for a limb to be re-expressed. The retention of such programs is, of course, evidence that this animal evolved from limbed ancestors.
It would be interesting to know what triggered this change. It’s not likely to be genetic (the asymmetry suggests that), but is probably a consequence of some pollutants that disrupt development. It’s not a good sign, anyway.
Some good suggestions from the comments: it may not even be a teratogenic deformity. It could just be a poor lizard that punched a claw through the abdominal wall as it was being digested, and the snake was briefly trundling about in pain from the injury.
We need to do a dissection!
We miss something important when we just look at the genome as a string of nucleotides with scattered bits that will get translated into proteins — we miss the fact that the genome is a dynamically modified and expressed sequence, with patterns of activity in the living cell that are not readily discerned in a simple series of As, Ts, Gs, and Cs. What we can’t see very well are gene regulatory networks (GRNs), the interlinked sets of genes that are regulated in a coordinated fashion in cells and tissues.
PLoS has recently published a highly speculative but very interesting paper on how a particular signaling pathway, the Hedgehog pathway, might have evolved. It’s at a fairly early stage in hypothesis testing, which is one of the things that makes it interesting — usually all you see published is the product of a great deal of data collection and experiment and testing, which means the scientific literature gives a somewhat skewed view of the process of science, letting the outsider mainly see work that has been hammered and polished, while hiding the rougher drafts that would better allow us to see how the story started and was built. It’s informative in particular for those who follow the creationist “literature”, which often crudely apes the products of actual working science, but lacks the sound methodological underpinnings. In particular, creationism completely misses the process of poking at the real world to develop ideas, since they begin with their conclusion.
So take this description as a work in progress — we’re seeing the dynamic of building up a good working model. As usual, it starts on a sound foundation of confirmed, known evidence, makes a reasonably hypothesis on the basis of the facts, and then proposes a series of research avenues with predicted results that would confirm the idea.
It’s sad to see that we’ve lost Brian Goodwin, one of the genuinely original (but not always right!) thinkers of our time. There aren’t many left of the old structuralist tradition in biology, the kind of non-genetic purists who tried to analyze development in terms of the fundamental physical and chemical properties of the organism—they’ve been swallowed up and lost in a triumphal molecular biology research program.
Edge has a nice interview with and essay by Goodwin — they’re good places to start. If that whets your appetite, you should also read his book, How the Leopard Changed Its Spots : The Evolution of Complexity(amzn/b&n/abe/pwll), which is aimed at general audiences and is a good overview of why we should look at more than just genes to explain form.
He was an advocate for one view of nature, and I think he missed the mark by neglecting genes as much as he did; we know now that a lot of details of morphology are directly affected in subtle and not-so-subtle ways by the genetics of the organism. But I think we can also make a case that the modern molecular biological approach is also missing a significant element. Every biologist ought to read a little Goodwin, just to leaven their picture of how biology works with his special perspective.
No, not really — my title is a bit of a sensationalistic exploitation of the thesis of a paper by Peterson, Dietrich, and McPeek, but I can buy into their idea that microRNAs (miRNAs) may have contributed to the pattern of metazoan phylogenies we see now. It’s actually a thought-provoking concept, especially to someone who favors the evo-devo view of animal evolution. And actually, the question it answers is why we haven’t had thousands of Cambrian explosions.
In case you haven’t been keeping up, miRNAs are a hot topic in molecular genetics: they are short (21-23 nucleotides) pieces of single stranded RNA that are not translated into protein, but have their effect by binding to other strands of messenger RNA (mRNA) to which they complement, effectively down-regulating expression of that messenger. They play an important role in regulating the levels of expression of other genes.
One role for miRNAs seems to be to act as a kind of biological buffer, working to limit the range of effective message that can be operating in the cell at any one time. Some experiments that have knocked out specific miRNAs have had a very interesting effect: the range of expressed phenotypes for the targeted message gene increases. The presence or absence of miRNA doesn’t actually generate a novel phenotype, it simply fine-tunes what other genes do — and without miRNA, some genes become sloppy in their expression.
This talk of buffering expression immediately swivels a developmental biologist’s mind to another term: canalization. Canalization is a process that leads organisms to produce similar phenotypes despite variations in genotype or the environment (within limits, of course). Development is a fairly robust process that overcomes genetic variations and external events to yield a moderately consistent outcome — I can raise fish embryos at 20°C or at 30°C, and despite differences in the overall rate of growth, the resultant adult fish are indistinguishable. This is also true of populations in evolution: stasis is the norm, morphologies don’t swing too widely generation after generation, but still, we can get some rapid (geologically speaking) shifts, as if forms are switching between a couple of stable nodes of attraction.
Where the Cambrian comes into this is that it is the greatest example of a flowering of new forms, which then all began diverging down different evolutionary tracks. The curious thing isn’t their appearance — there is evidence of a diversity of forms before the Cambrian, bacteria had been flourishing for a few billion years, etc., and what happened 500 million years ago is that the forms became visible in the fossil record with the evolution of hard body parts — but that these phyla established body plans that they were then locked into, to varying degrees, right up to the modern day. What the authors are proposing is that miRNAs might be part of the explanation for why these lineages were subsequently channeled into discrete morphological pathways, each distinct from the other as chordates and arthropods and echinoderms and molluscs.
Chalfie is interested in sensory mechanotransduction—how are mechanical deformations of cells converted into chemical and electrical signals. Examples are touch, hearing, balance, and proprioception, and (hooray!) he references development: sidedness in mammals is defined by mechanical forces in early development. He studies this problem in C. elegans, in which 6 of 302 nerve cells detect touch. It’s easy to screen for mutants in touch pathways just by tickling animals and seeing if they move away. They’ve identified various genes, in particular a protein that’s involved in transducing touch into a cellular signal.
They’ve localized where this gene is expressed. Most of these techniques involved killing, fixing, and staining the animals. He was inspired by work of Shimomura, as described by Paul Brehm that showed that Aequorin + Ca++ + GFP produces light, and got in touch with Douglas Prasher, who was cloning GFP, and got to work making a probe that would allow him to visualize the expression of interesting genes. It was a gamble — no one knew if there were additional proteins required to turn the sequence into a glowing final product…but they discovered that they could get functional product in bacteria within a month.
They published a paper describing GFP as a new marker for gene expression, which Science disliked because of the simple title, and so they had to give it a cumbersome title for the reviewers, which got changed back for publication. They had a beautiful cover photo of a glowing neuron in the living animal.
Advantages of GFP: heritable, relatively non-invasive, small and monomeric, and visible in living tissues. Roger Tsien worked to improve the protein and produce variants that fluroesced at different wavelengths. There are currently at least 30,000 papers published that use fluroescent proteins, in all kinds of organisms, from bunnies to tobacco plants.
He showed some spectacular movies from Silverman-Gavrila of dividing cells with tubulin/GFP, and another of GFP/nuclear localization signal in which nuclei glowed as they condensed after division, and then disappeared during mitosis. Sanes and Lichtman’s brainbow work was shown. Also cute: he showed the opening sequence of the Hulk movie, which is illustrated with jellyfish fluorescence (he does not think the Hulk is a legitimate example of a human transgenic.)
Finally, he returned to his mechanoreceptor work and showed the transducing cells in the worm. One of the possibilities this opened up was visual screening for new mutants: either looking for missing or morphologically aberrant cells, or even more subtle things, like tagging expression of synaptic proteins so you can visually scan for changes in synaptic function or organization.
He had a number of questions he could address: how are mechanotransducers generated, how is touch transduced, what is the role of membrane lipids, can they identify other genes important in touch, and what turns off these genes?
They traced the genes involved in turning on the mec-3 gene; the pathway, it turned out, was also expressed in other cells, but they thought they identified other genes involved in selectively regulating touch sensitivity. One curious thing: the mec genes are transcribed in other cells that aren’t sensitive, but somehow are not translated.
They are searching for other touch genes. The touch screen misses some relevant genes because they have redundant alternatives, or are pleiotropic so other phenotypes (like lethality) obscure the effect. One technique is RNAi, and they made an interesting observation. Trying about 17000 RNAis, they discovered that 600 had interesting and specific effects, 1100 were lethal, and about 15,000 had no effect at all. The majority of genes are complete mysteries to us. They’ve developed some techniques to get selective incorporation of RNAis into just neurons of C. elegans, so they’re hoping to uncover more specific neural effects. One focus is on the integrin signaling pathway in the nervous system, which they’ve knocked out and found that it demolishes touch sensitivity — a new target!
They are now using a short-lived form of GFP that shuts down quickly, so they’ve got a sharper picture of temporal patterns of gene activity.
Chalfie’s summary:
Scientific progress is cumulative.
Students and post-docs are the lab innovators.
Basic research is essential. Who would have thought working on jellyfish would lead to such powerful tools?
All life should be studied; not just model organisms.
Chalfie is an excellent speaker and combined a lot of data with an engaging presentation.
