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The problem with evo devo

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Last week, I gave a talk at UNLV titled "A counter-revolutionary history of evo devo", and I'm afraid I was a little bit heretical. I criticized my favorite discipline. I felt guilty the whole time, but I think it's a good idea to occasionally step back and think about where we're going and where we should be going. It's also part of some rethinking I've been doing lately about a more appropriate kind of research I could be doing at my institution, and what I want to be doing in the next ten years. And yes, I want to be doing evo devo, so even though I'm bringing up what I see as shortcomings I still see it as an important field.

I think of myself as primarily a developmental biologist, someone who focuses on processes in embryos and is most interested molecular mechanisms that generate form and physiology. But I'm also into evolution, obviously, and recently have been trying to educate myself on ecology. And this is where the conflicts arise. Historically, there has been a little disaffection between evolution and development, and we can trace it right back to Richard Goldschmidt and the neo-Darwinian synthesis.

I've been guilty of teaching bean-bag genetics this semester. Bean-bag genetics treats individuals as a bag of irrelevant shape containing a collection of alleles (the "beans") that are sorted and disseminated by the rules of Mendel, and at its worst, assigns one trait to one allele; it's highly unrealistic. In my defense, it was necessary — first-year students struggle enough with the basic logic of elementary transmission genetics without adding great complications — and of course, in some contexts, such as population genetics, it is a useful simplification. It's just anathema to anyone more interested in the physiological and developmental side of genetics.

The heart of the problem is that it ignores the issue of translating genotype into phenotype. If you've ever had a basic genetics course, it's quite common to have been taught only one concept about the phenotype problem: that an allele is either dominant, in which case it is expressed as the phenotype, or it's recessive, in which case it is completely ignored unless it's the only allele present. This idea is so 19th century — it's an approximation made in the complete absence of any knowledge of the nature of genes.

I have read the entirety of Hamza Andreas Tzortzis' paper, Embryology in the Qur'an: A scientific-linguistic analysis of chapter 23: With responses to historical, scientific & popular contentions, all 58 pages of it (although, admittedly, it does use very large print). It is quite possibly the most overwrought, absurdly contrived, pretentious expansion of feeble post hoc rationalizations I've ever read. As an exercise in agonizing data fitting, it's a masterpiece.

Here, let me give you the short version…and I do mean short. This is a paper that focuses with obsessive detail on all of two verses from the Quran. You heard me right: the entirety of the embryology in that book, the subject of this lengthy paper, is two goddamned sentences, once translated into English.

We created man from an essence of clay, then We placed him as a drop of fluid in a safe place. Then We made that drop of fluid into a clinging form, and then We made that form into a lump of flesh, and We made that lump into bones, and We clothed those bones with flesh, and later We made him into other forms. Glory be to God the best of creators.

Seriously, that's it. You have just mastered all of developmental biology, as taught by Mohammed.

ResearchBlogging.org“The Selfish Gene.” “Selfish DNA.” Oh, how such phrases can get people bent out of shape.  Stephen Jay Gould hated such talk (see a little book called The Panda’s Thumb), and Richard Dawkins devoted more time to answering critics of his use of the term ‘selfish’ than should have been necessary. Dawkins’ thesis was pretty straightforward, and he provided real examples of “selfish” behavior of genes in both The Selfish Gene and its superior sequel, The Extended Phenotype. But there have always been critics who can’t abide the notion of a gene behaving badly.

Leaving aside silly bickering about the attribution of selfishness or moral competence to little pieces of DNA, let’s consider what we might mean if we tried to imagine a really selfish piece of DNA. I mean a completely self-centered, utterly narcissistic little piece of DNA, one that not only seeks its own interest but does so with rampant disregard for other pieces of DNA and even for the organism in which it travels. Can we imagine, for example, a piece of DNA that deliberately harms its host in order to propagate itself?

That's not hyperbole. I really mean it. How else could I react when I open up the latest issue of Bioessays, and see this: Cephalopod origin and evolution: A congruent picture emerging from fossils, development and molecules. Just from the title alone, I'm immediately launched into my happy place: sitting on a rocky beach on the Pacific Northwest coast, enjoying the sea breeze while the my wife serves me a big platter of bacon, and the cannula in my hypothalamus slowly drips a potent cocktail of cocain and ecstasy direct into my pleasure centers…and there's pie for dessert. It's like the authors know me and sat down to concoct a title where every word would push my buttons.

The content is pretty good, too. It's not perfect; the development part is a little thin, consisting mainly of basic comparative embryology of body plans, with nothing at all really about deployment of and interactions between significant developmental genes. But that's OK. It's in the nature of the Greatest Science Papers Ever Written that stuff will have to be revised and some will be shown wrong next month, and next year there will be more Greatest Science Papers Ever Written — it's part of the dynamic. But I'll let it be known, now that apparently the scientific community is aware of my obsessions and is pandering to them, that the next instantiation needs more developmental epistasis and some in situs.

This paper, though, is a nice summary of the emerging picture of cephalopod evolution, as determined by the disciplines of paleontology, comparative embryology, and molecular phylogenetics, and that summary is internally consistent and is generating a good rough outline of the story. And here is that story, as determined by a combination of fossils, molecular evidence, and comparative anatomy and embryology.

A little cis story

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I found a recent paper in Nature fascinating, but why is hard to describe — you need to understand a fair amount of general molecular biology and development to see what's interesting about it. So those of you who already do may be a little bored with this explanation, because I've got to build it up slowly and hope I don't lose everyone else along the way. Patience! If you're a real smartie-pants, just jump ahead and read the original paper in Nature.

A little general background.

svbmap.gif

Let's begin with an abstract map of a small piece of a strand of DNA. This is a region of fly DNA that encodes a gene called svb/ovo (I'll explain what that is in a moment). In this map, the transcribed portions of the DNA are shown as gray shaded blocks; what that means is that an enzyme called polymerase will bind to the DNA at the start of those blocks and make a copy in the form of RNA, which will then enter the cytoplasm of the cell and be translated into a protein, which does some work in the activities of that cell. So svb/ovo is a small piece of DNA which, in the normal course of events, will make a protein.

ResearchBlogging.orgGiven that disputes over the existence and meaning of the phylotypic stage and the hourglass model have simmered in various forms for a century and a half, the remarkable correspondence between the hourglass model and gene expression divergence discovered by Kalinka and Varga and colleagues would be big news all by itself. But amazingly, that issue of Nature included two distinct reports on the underpinnings of the phylotypic stage. The other article involved work in another venerable model system in genetics, the zebrafish.

The report is titled "A phylogenetically based transcriptome age index mirrors ontogenetic divergence patterns" and is co-authored by Tomislav Domazet-Loso and Diethard Tautz. To understand how their work has shed light on the phylotypic stage and the evolution of development, we’ll need to look first at an approach to the analysis of evolutionary genetics that these two scientists pioneered: phylostratigraphy.

So, shortly after the first post on the hourglass model went up here on the Panda’s Thumb, the senior author of one of the two featured papers (the article using fruit flies, titled "Gene expression divergence recapitulates the developmental hourglass model") contacted me, clearly enthused about our interest in the story. He’s Pavel Tomancak, and together with the co-first author on the study, Alex Kalinka, he offered some useful feedback as well as some cool images. Here are some of their further thoughts, posted with their permission and edited slightly by me. Let’s think of them as honored guest bloggers.

ResearchBlogging.org The controversy about the existence of the phylotypic stage is more than some bickering about whether one blobby, slimy fish-thing looks more like a Roswell alien than another one does. It’s about whether the phylotypic stage means something, whether it tells us something important about development and how developmental changes contribute to evolution. To answer such a question, we need more than another set of comparisons of the shape and movements of embryos and their parts. We need a completely different way of looking at the phylotypic stage, to see if something notable is going on under the hood. So vertebrates all look the same at the tailbud stage. What does that mean?

Embryos look the way they do because of the positions and behaviors of the cells that make them up. The cells in an embryo all have the same DNA, and the link between that DNA and those specific cell behaviors is the basic process of gene expression. (This is a fundamental principle of developmental biology.) And by gene expression, we usually mean the synthesis of messenger RNA under the direction of genes in the DNA. Different cell types express different sets of genes, and the orchestration of the expression of particular genes at particular times is a big part of what makes development happen. When considering the phylotypic stage, then, developmental biologists wondered: is the apparent similarity of embryos at that stage reflected by similarities in gene expression. Or, more specifically, does the hourglass model hold up when we look at gene expression? This was the focus of the two articles in last Friday’s Nature that inspired the cool cover.

Disputes and controversies in science are always a good thing. They're fun to read about (and to write about), and they're bellwethers of the health of the enterprise. Moreover, they tend to stimulate thought and experimentation. Whether scientists are bickering about evo-devo, or about stem cells in cancer, or about prebiotic chemistry, and whether or not the climate is genial or hostile, the result is valuable.

Now of course, some controversies are invented by demagogues for political purposes. The dispute in such cases is far less interesting and clearly less profitable, even if participation by scientists is necessary.

This week, two papers in Nature weighed in on a major scientific controversy that has its roots in pre-Darwin embryology, fueled by some gigantic scientific personalities and even tinged with what some would call fraud. This intense scientific dispute spawned a sort of doppelganger, a manufactured controversy that is just one more invention of anti-evolution propagandists. The Nature cover story gives us a great opportunity to look into the controversies, real and imagined, and to learn a lot about evolution and development and the things we're still trying to understand about both.

The scientific dispute is an old one, dating to when scientists first began to study embryonic development in earnest. Embryologists like the great Karl Ernst von Baer noticed that the embryos of very different animals often looked so similar that they could hardly be distinguished from each other. A chicken embryo, at some point, looks an awful lot like a human embryo. What does this mean? Two schools of thought (roughly speaking) entered into competition, with evolution as the major subtext. One set of ideas envisioned development as recapitulation: development was a sort of re-play of evolution, with the organism recapitulating its evolutionary history as it took shape. Recapitulation theory was the brainchild of Ernst Haeckel, whose view of development was codified as his Biogenetic Law and sloganeered as "Ontogeny recapitulates phylogeny." Against recapitulation were the views of von Baer and others; von Baer formulated his own set of laws, the third of which repudiates recapitulation rather directly. Everyone agreed that embryos of different animals often looked quite alike; the dispute was about what this meant. And it seems that those who opposed evolutionary explanations (like von Baer) were eager to point to difference and divergence during development, while those who championed evolutionary views wanted to emphasize the shocking similarities between, say, chickens and mammals when compared at key embryological junctures.

Haeckel, famously, went on to point to those similarities as evidence for common ancestry and, infamously, to create a certain illustration of that evidence. His picture, thought by even some embryologists to be partly fraudulent (more accurately, "doctored"), is now a staple of anti-evolution propaganda. You can read all about that elsewhere; suffice it to say that Haeckel's drawings have long since been "corrected" without creating any problems for evolutionary theory. (For a much more detailed treatment of this saga, see Richardson and Keuck, Biological Reviews, 2002.)

RichardsonPhylotypicLineupFromGilbert300px.jpg

But interestingly, the debates about recapitulation morphed (wink) over the years into a distinct but related disagreement about whether animal development passes through a stage that is common to - or typical of - the lineage of the organism. Because although Haeckel's recapitulation idea didn't survive, it remained clear that development seemed to reflect evolutionary commonalities. Consider the photos on the right. (The figure was created by Michael K. Richardson, who led the research group that critiqued Haeckel's drawings in 1998.) While the various embryos shown all end up looking quite different - looking like the adult form, in other words - they seem to "start" at a place that's notably similar. (Compare the embryos in the first row.) That starting point is not the beginning of development, and in fact those different kinds of embryos got to that starting point via rather different beginnings. In other words, it seems that animal embryos pass through roughly three phases of development: an early phase that can vary from group to group (say, between birds and mammals), a late phase in which group-specific forms are established, and a middle phase that is eerily similar among groups. That middle phase has come to be known as the "phylotypic stage" of development, meaning that it is a stage at which the embryo looks like a typical example of its evolutionary group. For insects, this is thought to be the "extended germband" stage; for vertebrates, it's roughly the tailbud stage. The point is that there is a middle phase of development during which animal embryos of varying morphological destinies look very similar, even if their earlier stages seemed very distinct. This model of developmental trajectories, compared across groups, is known as the "hourglass model," nicely depicted by Richardson and colleagues in the cartoon on the left.

HourglassModelCartoonRichardson-etal250px.gif

Why all the controversy? Well, the disputes all seem to be related to the fact that the model is mostly descriptive. And so, one criticism is that the model is based on what embryos look like, and not strongly anchored in carefully-defined and -measured characters. Moreover, some critics have noted that the comparisons were often restricted to popular laboratory species, such that when the analysis was expanded to include a broader set of species, the similarities in the waist of the hourglass become less striking. In other words, the dispute centered on the basis of the model. Critics were disputing the very existence of the phylotypic stage.

Oh, and while this interesting scientific debate was ongoing, some propagandists were shadowboxing with Haeckel's ghost, shrieking about fraud while creating in the minds of their dupes the illusion of a different debate: one about whether development and evolution are conceptually linked. Along the way, these busy demagogues suggested that the phylotypic stage is an illusion, cherry-picking their data more shamelessly than Haeckel ever did. In any case, these folks were exploiting the real scientific dispute: whether the phylotypic stage can be defined more rigorously, in a way that links the similarities (whatever they are) to common ancestry.

NatureCoverPhylotypic.jpg

And that brings us to the cover story in this week's issue of Nature. The cover image depicts a version of Haeckel's infamous illustration. The issue includes two reports, very different in their approach and in the animals they examined. Both reports provide striking support for the hourglass model, by showing that the phylotypic stage is indeed characterized by distinctive and fascinating patterns of gene expression. Part II will explore those two papers.

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Image credits: 1) embryo images from Gilbert, Developmental Biology, 6th Edition, online at PubMed; 2) cartoon from Richardson et al. 1998.

ResearchBlogging.orgRandomness. Shakespeare referred to it. The Bible talks about it. People love to bicker about what it really is, or whether it truly exists. And creationists, especially those of the ID subspecies, consider it a fighting word. A random process, many would say, is a process that doesn't involve God, or direction, or intention, or whatever it is that the culture warriors of the Discovery Institute are so foolishly fighting for. Ah, but it's not just the propagandists of design-think who can mistakenly assume that an ordered process is "directed." Consider this tale of a random process being put to surprising use during vertebrate embryonic development.

Our story comes from Nature about a month ago, and I will present it in four acts.

Act I: The elongation of an embryo

We all know that animal embryos acquire their form through various morphings and twistings. One interesting example is axis elongation, which is just what it sounds like: the embryo stretches out until it clearly has a long axis, then continues to elongate to form something with a head and a tail and everything in between. But "stretch" is a poor term for what's really happening: the tail end of the embryo is growing while the structures closer to the head are beginning to develop into recognizable structures. Developmental biologists know that new cells are added near the tail end, and we know that various directed processes control many similar movements during early development. It was reasonable to assume that these mechanisms would account for embryo elongation, but the actual processes were unknown before the experiments of Bénazéraf and colleagues ("A random cell motility gradient downstream of FGF controls elongation of an amniote embryo," Nature 8 July 2010).

ChickStage11.jpg

The authors employed an old warhorse of developmental biology, the chick embryo. At stage 11, the embryo looks nothing like the animal it will become; it has a head-like thing at one end (the top in the picture on the right), a weird hole at the bottom (Hensen's node), and some blocky structures called somites in between. Down at the bottom, on either side of the hole, is a tissue called the presomitic mesoderm (PSM). The anatomical details needn't concern us; what matters is that we understand that the embryo is elongating toward the bottom, that cells are being made near the top of that hole and that they are moving toward the tail, making it grow. Curious about how this works, Bénazéraf and colleagues started deleting pieces of the tail-end of the embryo, and they found that the PSM was critical for elongation. Good to know.

Act II: Cell movements in the elongating embryo

So, what's going on in the PSM that causes elongation? The authors used a nifty technique called electroporation to label the cells in that region so they could watch them as the embryo grew. Basically, they used an electric field to introduce DNA into the cells of interest the day before; the DNA caused the cells to express the wonderful and famous green fluorescent protein (GFP) so that individual cells could be monitored as the embryo continued to develop in culture outside of the egg. They found something interesting: near the tail of the embryo, the PSM cells were more motile than they were near the front of the PSM. But the cells near the front were more packed together. So try to picture it: in this region on either side of the center of the tail end of the embryo is an area (the PSM) of cells that are moving more frantically near the tail and that are more packed together toward the head. It would seem as though the cells are busily moving toward the tail, and that they get less crowded and more mobile as they get there. And when the authors looked at movement of individual cells, sure enough, there was a directional bias in the movement, meaning simply that cells in the PSM tended to move toward the tail. It looks like a simple case of directed migration of cells toward a target. Interesting, maybe, but not such big news. But then, a noise from the next room. Exeunt.

Act III: Random cell movements in the elongating embryo

So cells seem to move toward the tail. This could mean they're being directed toward the tail by some kind of homing mechanism, and this would be a reasonable expectation. But because the embryo is elongating, it could be that the directed movement of individual cells is an illusion: the cells are moving toward the tail because the space they inhabit is moving toward the tail. The authors addressed this by cancelling out the effect of elongation of the cells' environment, and focusing solely on the movement of cells within that environment. The environment in this case is the extracellular matrix, or ECM, as indicated by one of its components, fibronectin. I'm sorry about the jargon, but I included it so I could quote the authors in full as they describe the results of the experiment:

Surprisingly, the movements of cells relative to the ECM did not show any local directional bias. The mean square displacement of these cells compared to the fibronectin movement scales with time, indicating that cells exhibit a 'random walk'-like diffusive behaviour, with the diffusion of cells relative to the fibronectin following a posterior-to-anterior [back-to-front] gradient.

In other words, the cells are moving randomly, behaving like molecules diffusing in a liquid. The authors verified this by looking at cell protrusions, the telltale signs of a cell's migrational direction. The protrusions all pointed in random directions. Amazingly, this seemingly ordered march of cells toward the back, resulting in the growth of the tail end of the embryo, is the product of random cell movement. And yet it yields an ordered result. How?

Act IV: A gradient of random cell movement controlled by a conserved developmental signaling system

Recall that cell movement in the PSM is not uniform: cells near the tail move (randomly) more. The authors knew that an ancient and well-known signaling system functions in a similarly graded fashion in that tissue. Known as the FGF/MAPK pathway, it's fairly simple to manipulate experimentally. Bénazéraf and colleagues found that whether they turned the signaling up or down, the result was the same: elongation was stunted. This might seem strange, but it makes perfect sense: it's the graded nature of the signaling that matters, so turning it all the way up or all the way down erases the gradient and leads to the same result. What matters, for elongation, is that random cell movement is greater in the back than in the front. This leads to elongation, because the tail end contains cells that move more and have more freedom of motion due to their being less tightly packed.

The upshot is that an ancient conserved signaling system causes a simple gradient of random movement which, in the presence of physical constraints, leads necessarily to elongation of the embryo in one direction. It looks for all the world like homing or some other directed migration, but it's not. And, intriguingly, the authors conclude by suggesting that the mechanism might be quite common in the biosphere:

Axis formation by outgrowth is a common morphogenetic strategy that is widely evident in animals and plants. Thus, the mechanism described here might apply to other well-characterized, polarized axes, such as the limb buds, in which a similar FGF/MAPK gradient is established along the proximo-distal axis.

Randomness. Learn to love it. The End.

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Image credit: "Normal stages of chick embryonic development," poster on Developmental Dynamics site

Bénazéraf, B., Francois, P., Baker, R., Denans, N., Little, C., & Pourquié, O. (2010). A random cell motility gradient downstream of FGF controls elongation of an amniote embryo Nature, 466 (7303), 248-252 DOI: 10.1038/nature09151

ResearchBlogging.org

Mutate. Select. Repeat. Mutate. Select. Repeat. You can’t understand evolutionary biology if you don’t get the significance of that process. And yet, if you think that’s all there is to it, you’re way off track. PZ explained this very nicely here last week. Let’s focus on one simple point that he made, and look at some recent and significant work on that subject that shows just how misleading some of the common simplifications of evolutionary biology can become.

Here’s PZ on simple views of mutation and selection:

Stop thinking of mutations as unitary events that either get swiftly culled, because they’re deleterious, or get swiftly hauled into prominence by the uplifting crane of natural selection. Mutations are usually negligible changes that get tossed into the stewpot of the gene pool, where they simmer mostly unnoticed and invisible to selection.

I think this is an extremely important point, both for those seeking to answer creationist propaganda and for anyone else trying to understand the process of evolutionary change. The common picture, painted all too often by commentators of various stripes, depicts a world in which mutations run a harrowing gauntlet of selection that is likely to foolishly discard both the gems and the proto-gems of biological function. Oh sure, the cream eventually rises to the top, but only through the magic of seemingly endless eons and limitless opportunities. I hope that most readers of the Panda’s Thumb are annoyed by this crude caricature, but it’s the standard tale, and when the narrator only has a paragraph, it’s the one we’re most likely to hear.

To improve the situation, we might first add the concept of random drift. And that helps a lot. Then we would emphasize the selective neutrality of the vast majority of all mutations, as PZ did. And that helps a lot, too. Let’s look at another helpful concept, one from the evo-devo playbook, almost crazy at first glance but remarkably interesting and important.

Suppose that one reason many mutations are selectively near-neutral is because genetic systems are able to tolerate mutations that have the capacity to be strongly deleterious. Suppose, in other words, that organisms are robust enough to live with seriously nasty genetic problems. This would mean that such mutations could escape selection, and that populations could harbor even more genetic diversity than our simplistic account would seem to suggest.

Some very nice work in the fruit fly (“Phenotypic robustness conferred by apparently redundant transcriptional enhancers”), performed by Frankel and colleagues and published in Nature in July, shows us one way this sort of thing can work. The authors were studying genetic control elements (called enhancers) that turn genes on and off. Specifically, they were looking at how the expression of a gene called shavenbaby was affected by a set of enhancers. (The shavenbaby gene controls the development of hair-like structures on the surface of the fly larva - i.e., maggot - and so alterations in the embryo’s patterning that result from changes in shavenbaby function are easily detectable by simple microscopy.) Now, like many genes that control development, shavenbaby is regulated by a few different enhancers, some that are close to the gene and others that are apparently redundant and are further away. These latter elements are called “shadow” enhancers, as they are remote and distinct from the primary enhancers but highly similar in activity.

Why all this redundancy? Others had proposed that shadow enhancers might confer “phenotypic robustness” - i.e., developmental or functional robustness - by maintaining function in the face of significant challenges (environmental changes, for example), and Frankel et al. set out to test that hypothesis. First they deleted the shadow enhancer region, and this had a very mild effect, consistent with the idea that the shadow enhancers are redundant with respect to the function of the primary enhancers. But then they examined development in the absence of the shadow enhancers, now introducing environmental stress (extremes of temperature), and found dramatic developmental defects. They concluded that the shavenbaby shadow enhancers normally contribute to phenotypic robustness through what they term “developmental buffering.” In other words, the animal’s critical developmental pathways are buffered against many disastrous alterations, in part through the action of redundant control systems.

That’s interesting all by itself, but the authors went one crucial step further. What if the redundant enhancers can also buffer against genetic disasters? The experiment was straightforward: they deleted one copy of a major developmental control gene (called wingless). Those animals are just fine, until they lose the buffering of the shavenbaby shadow enhancers. Without the redundant system, the loss of one wingless gene leads to a significant change in developmental patterning. The conclusion, I think, is quite interesting: the impact of the shadow enhancers only becomes apparent when the system is stressed, by environmental challenges and even by genetic problems elsewhere in the genome.

Such developmental buffering systems are thought to be common in animal genomes, and this means that animal development is capable of tolerating significant genetic dysfunction. It means, I think, that simplistic stories about deleterious mutants being readily discarded from populations are even less useful than we already should have realized, and that’s without the deliberate misuse of such outlines by anti-evolution spinmeisters.

And one last thing. Why my little comment about the evo-devo playbook? Well, one concept championed by evo-devo thinkers is the notion of “evolvability.” The idea (roughly) is that the ability to generate diversity is something that we should expect to see in evolution. Like most other evo-devo proposals, it’s been savaged by some smart critics. But phenotypic buffering by redundant developmental control elements is just the kind of thing that “evolvability” was meant to encompass when it was discussed by Kirschner and Gerhart more than a decade ago. So I say we give credit where it’s due. Anyone else?

Several years ago, I saw a fantastic talk at the Evolution meeting about Intraspecific macroevolution: variation of cranial shape in dog breeds. The talk was by Abby Drake, then a grad student, and reported on a huge digital morphometric comparison of the skulls of dogs and many representatives from the order Carnivora (dogs, cats, bears, sea lions, etc.).

Morphometrics basically consists of taking digital photos of e.g. bones from different angles, and then marking the same landmarks on homologous bones across a big group. Then you can quantitatively compare the differences in shape, independent of things like body size. This is a much more sophisticated analysis than is possible with just calipers, where you can only get length, width, etc.

No metazoan is an island

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I'm one of those dreadful animal-centric zoologically inclined biologists. Plants? What are those? Fungi? They're related to metazoans somehow. Lichens? Not even on the radar. The first step in fixing a problem, though, is recognizing that you have one. So I confess to you, O Readers, that my name is PZ, and I am a metazoaphile. But I can get better.

My path to opening up to wider horizons is to focus on what I find most interesting about animals, and that is that they are networks of cells driven by networks of genes that generate patterned responses of expression by cell signaling, or communication. See? I'm already a little weird. Show me a baby bunny, and I don't just see a cute little furry pal with an adorable twitchy nose, I see an organized and coherent array of differentiated tissues that arose by a temporal sequence of cell-cell interactions, and I just wanna open him up and play with his widdle epithelial sheets and dismantle his pwetty ducts and struts and fibers and fluids, oochy coo. And ultimately, I want to take apart each cell and ask why it has its particular assortment of genes switched off and on, and how its state affects its neighbors and the whole of the organism.

Which means, lately, that I've acquired a growing interest in bacteria. If I were 30 years younger, I could probably be seduced into a career in microbiology.

There are a couple of reasons why an animal-centric biologist would be interested in bacteria. One is the principle of it; the mechanisms that animal cells use to build complex arrangements of tissues were all first pioneered in single-celled organisms. We have elaborated and added details to gene- and cell-level phenomena, but it's a collection of significant quantitative differences, with nothing known that is essentially new in metazoan cells. All the cool stuff was worked out by evolution in the 3-4billion years before the Cambrian, a potential that simply blossomed in the past half-billion years into big conglomerations of cells. Understanding how the building blocks of multicellularity work individually ought to be a prerequisite to understanding how the assemblages work.

But there's another reason, too, a difference in perspective. It is our conceit to regard ourselves as individuals of Homo sapiens, a body of cells clonally derived from a single human cell. It's not true. It turns out that each one of us is actually a whole population of species, linked by our evolutionary history and lumbering through the world as a team. Genus Homo is also genera Escherichi and Bacteroidetes and Firmicutes and many others.

schematic.jpeg

How to make a snake

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Blogging on Peer-Reviewed Research

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.

Sean Carroll live web talk

As part of a year-long Darwin Lecture Series, evo-devo guy Sean Carroll will be giving a webcast talk based around his Making of the Fittest. The talk is on Wednesday, November 4, and you can sign up for the live webcast here.

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 horsepuckey. 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.

Blogging on Peer-Reviewed Research

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.

darwinopterus.jpeg
(Click for larger image)

Figure 2. Holotype ZMNH M8782 (a,b,e) and referred specimen YH-2000 ( f ) of D. modularis gen. et sp. nov.: (a) cranium and mandibles in the right lateral view, cervicals 1-4 in the dorsal view, scale bar 5cm; (b) details of the dentition in the anterior tip of the rostrum, scale bar 2cm; (c) restoration of the skull, scale bar 5cm; (d) restoration of the right pes in the anterior view, scale bar 2 cm; (e) details of the seventh to ninth caudal vertebrae and bony rods that enclose them, scale bar 0.5 cm; ( f ) complete skeleton seen in the ventral aspect, except for skull which is in the right lateral view, scale bar 5 cm. Abbreviations: a, articular; cr, cranial crest; d, dentary; f, frontal; j, jugal; l, lacrimal; ldt, lateral distal tarsal; m, maxilla; mdt, medial distal tarsal; met, metatarsal; n, nasal; naof, nasoantorbital fenestra; p, parietal; pd, pedal digit; pf, prefrontal; pm, premaxilla; po, postorbital; q, quadrate; qj, quadratojugal; sq, squamosal; ti, tibia.

Limusaurus inextricabilis

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Blogging on Peer-Reviewed Research

My previous repost was made to give the background on a recent discovery of Jurassic ceratosaur, Limusaurus inextricabilis, and what it tells us about digit evolution. Here's Limusaurus—beautiful little beastie, isn't it?

limusarus.jpeg
(Click for larger image)

Photograph (a) and line drawing (b) of IVPP V 15923. Arrows in a point to a nearly complete and fully articulated basal crocodyliform skeleton preserved next to IVPP V 15923 (scale bar, 5 cm). c, Histological section from the fibular shaft of Limusaurus inextricabilis (IVPP V 15924) under polarized light. Arrows denote growth lines used to age the specimen; HC refers to round haversian canals and EB to layers of endosteal bone. The specimen is inferred to represent a five-year-old individual and to be at a young adult ontogenetic stage, based on a combination of histological features including narrower outermost zones, dense haversian bone, extensive and multiple endosteal bone depositional events and absence of an external fundamental system. d, Close up of the gastroliths (scale bar, 2 cm). Abbreviations: cav, caudal vertebrae; cv, cervical vertebrae; dr, dorsal ribs; ga, gastroliths; lf, left femur; lfl, left forelimb; li, left ilium; lis, left ischium; lp, left pes; lpu, left pubis; lsc, left scapulocoracoid; lt, left tibiotarsus; md, mandible; rfl, right forelimb; ri, right ilium; rp, right pes; sk, skull.

What's especially interesting about it is that it catches an evolutionary hypothesis in the act, and is another genuine transitional fossil. The hypothesis is about how fingers were modified over time to produce the patterns we see in dinosaurs and birds.

Snails have nodal!

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Blogging on Peer-Reviewed Research

My first column in the Guardian science blog will be coming out soon, and it’s about a recent discovery that I found very exciting…but that some people may find strange and uninteresting. It’s all about the identification of nodal in snails.

nodal_guts.jpg

Why should we care? Well, nodal is a rather important — it’s a gene involved in the specification of left/right asymmetry in us chordates. You’re internally asymmetric in some important ways, with, for instance, a heart that is larger on the left than on the right. This is essential for robust physiological function — you’d be dead if you were internally symmetrical. It’s also consistent, with a few rare exceptions, that everyone has a stronger left ventricle than right. The way this is set up is by the activation of the cell signaling gene nodal on one side, the left. Nodal then activates other genes (like Pitx2) farther downstream, that leads to a bias in how development proceeds on the left vs. the right.

In us mammals, the way this asymmetry in gene expression seems to hinge on the way cilia rotate to set up a net leftward flow of extraembryonic fluids. This flow activates sensors on the left rather than the right, that upregulate nodal expression. So nodal is central to differential gene expression on left vs. right sides.

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