Jonathan MacLatchie collides with reality again

Jonathan MacLatchie, the creationist who challenged me to answer his questions about development in Glasgow, has posted his account of our encounter and his problems with evolution. It is completely unsurprising — he still doesn’t understand any of the points.

Of his 10 questions, 7 were quickly dismissable and were more than thoroughly addressed in my talk. They rest on a deep misconception that is shared with Jonathan Wells and many other pseudoscholarly creationists; I can summarize it with one standard template: “Since Darwinian evolution predicts that development will conserve the evolutionary history of an organism, how do you account for feature X which doesn’t fit that model?” To which I can simply reply, “Evolution does not predict that development will conserve the evolutionary history of an organism, therefore your question is stupid.” It doesn’t matter how many X’s he drags out, given that the premise is false, the whole question is invalid. But they can play that rhetorical game endlessly, citing feature after feature that doesn’t fit their misunderstanding of the science, making it sound to the clueless like they’ve got a legion of contradictions with evolution. Unfortunately for them, their objections are to creationist evolution, which has very little relationship to real evolution.

The gist of my talk was that Haeckel was wrong, that there was no recapitulation of developmental stages. Variation can and does occur at every stage of development; early and late stages vary greatly; evolution does not proceed primarily by terminal addition of new stages, as Haeckel postulated; but there is an interesting and real convergence on the broad, general outlines of the body plan at one point in development that needs to be explained.

MacLatchie’s response, greatly abbreviated, is to say that recapitulation doesn’t occur; variation occurs at every stage of development; early and late stages vary greatly; and look! I have papers from the peer-reviewed scientific literature that agree with me! Well, yes. That’s what I said. That is the conventional, ordinary, normal, well-understood, evolution-compatible side of the story from the scientists, like I’d been saying. Is there an echo in here, or do you just not understand what you heard or what you read, that you think the facts are evidence against evolution?

Apparently, in the Q&A for my talk (which you can now listen to; MacLatchie is first up), he asked me, I think, question #3 from his list, but I couldn’t really tell. As is typical, he turned it into a long-winded turgid mess, and I’ll be honest, I really couldn’t grasp what he was trying to ask, and I think he was actually getting at two different things. One is that there are differences in the embryological origins of some organs; this bothers him, apparently, because he’s sitting there expecting that there shouldn’t be any differences in how, for instance, the neural tube forms, because it’s a primitive structure, and therefore, because development is supposed to recapitulate evolution, they should be identical. I missed that; I was trying to see a more intelligent question in his verbiage. Now that I’ve read the papers he was waving around, I can answer a little differently: yes. There are differences in how different organs form in different species.

So?

It is not a tenet of evo-devo that primitive structures must follow identical ontogenetic pathways. We actually understand that divergence can occur at all stages of development.

The other thing he was getting at was something I thought I understood when I tried to get him to focus on one example, and suggested neural tube formation. There what we see despite differences between species is a widely conserved molecular homology — that there is an interplay between BMP and Dpp in defining the prospective nervous system in flies and vertebrates. These deep homologies in organization were not expected and not predicted by evolutionary biology, but their presence does imply evolutionary affinities. That there are differences — for instance, a frog will form a hollow tube by folding the sheet of the neural plate, while a fish seems to submerge the sheet into the body and then secondarily cavitate* — are real, but relatively superficial. And differences are not precluded by evolutionary theory!

I wish I could get that one thought into these guys heads: evolutionary theory predicts differences as well as similarities. Finding a difference between two species does not send us rocking back on our heels, shocked that such a thing could be.

There’s another weird thing in that clip that is so typical of creationists. He pointed at those papers of his, dropped a few scientists’ names, and claimed they all supported his position. They do not. He gave me copies of three of them afterwards; two I’d already read and was fairly familiar with. Come on, he was citing Pere Alberch, the great synthesizer of development and evolution, in support of intelligent design creationism?

MacLatchie doesn’t even understand the paper. What Alberch is doing in it is arguing that many efforts to use developmental information in systematics go wrong because they have a creeping Haeckelian interpretation, that the sequences of events in development should preserve the evolutionary sequence. They don’t, he said, and as I also said, Haeckelian recapitulation is false. So, once again, MacLatchie was confronting me with a paper that confirmed what I had said as if it somehow showed I was wrong. I really don’t get it.

It’s also a subtle example of quote-mining. In the paper, Alberch gives two examples of developmental variation in vertebrates, describing differences in toe number and in the mode of neural tube formation. MacLatchie quotes him this way:

According to the Alberch paper (the claims of which remain true to this day), it is noted that it is “the rule rather than the exception” that “homologous structures form from distinctly dissimilar initial states.”

First, it’s a slightly odd quote: the two phrases are from two different paragraphs, and are in the reverse order from how they’re written here. He doesn’t substantially change the meaning, though, so it’s not quite as nasty as the usual scrambling. (However, it is peculiar that this same exact cut & flip quote can also be found in the works of Harun Yahya, and who knows where he got it; it’s just another example of creationists copying each other.)

However, this is where it gets devious. MacLatchie omits to mention the very next sentence after part of that quote:

The diversity of tarsal morphology, as well as the variation in ontogenetic pathways leading to the formation of the neural tube, reflect variations in developmental parameters or initial conditions within conserved developmental programs. [emphasis mine] There is structural organization in this scheme that should be amenable to systematic analysis but the information in not in the ontogenetic sequence.

You see, that’s the point of his paper: it’s a criticism of naive interpretations of developmental processes that are built on Haeckelian assumptions that the sequence of stages will be evolutionarily conserved. They aren’t. This does not represent a denial of evolutionary relevance; quite the contrary, he goes on to propose better ways of examining the role of development. After giving some examples, he explains that better methods “share the common emphasis on regulation within a resilient developmental program, and they emphasize the need to go beyond the perception of ontogeny as a sequence of discrete developmental stages.”

It’s actually surprisingly offensive to see creationist citing the late Alberch as somehow supporting their lunatic views. I suddenly feel like I was not rude enough to MacLatchie at that talk.

It’s a superficial ploy creationists play. They don’t have any scientific literature of their own, so they go rummaging about in the genuine scientific literature and start pulling out fragments that show disagreement and questions in the evolutionary community. And that is so trivial to do, because they don’t grasp something obvious and fundamental: every science paper has as its throbbing heart a question and an argument. Seriously. Every single paper on evolution is arguing with evolution, probing and pushing and testing. I am not at all impressed when some clueless dingbat pulls up Alberch’s paper titled “Problems with the interpretation of developmental sequences” and crows about finding a paper that talks about “problems”. Problems are what we’re interested in.

In an attempt at turnabout, MacLatchie also tries to claim that I distorted Jonathan Wells’ position by implying that Wells does not try to use Haeckel’s errors to undermine the foundations of evolution, because Wells openly explains that Haeckel was discredited by his peers.

A casual reading of chapter 3 of Wells’ The Politically Incorrect Guide to Darwinism and Intelligent Design (which was cited by Myers) reveals that Wells, in fact, tells us that “Haekel’s fakery was exposed by his own contemporaries, who accused him of fraud, and it has been periodically re-exposed ever since.”

Why, yes, it’s part of Wells’ game. He declares that Haeckel’s theory has been thoroughly rubbished, and therefore the foundations of ‘Darwinism’ have been destroyed. Note the sneaky substitution: Haeckel’s theory is not the foundation of evolution. We can kill it, kick it when it’s down, run it through a woodchipper, and it just doesn’t matter — it’s not part of evolutionary theory. I’ve dealt with this subterfuge at length, so I don’t really need to go into it again, do I?

*Which has since been found to be less of a difference than thought before. The fish neural tube does fold, but the cells are more tightly adherent to one another so you don’t see the central ventricle forming as obviously.


I said 7 of the 10 questions are blown to smithereens by the simple fact that they are built on false premises — MacLatchie doesn’t really understand that Haeckelian recapitulation is not part of evolutionary theory. I’ll quickly answer the remaining three right here.

4) Could you please explain the near-total absence of evidence for evolutionarily relevant (i.e. stably heritable) large-scale variations in animal form, as required by common descent? “Near-total”, that is, because losses of structure are often possible. But common descent requires the generation of anatomical novelty. Why is it the case that all observed developmental mutations that might lead to macroevolution (besides the loss of an unused structure) are harmful or fatal?

This is just like the standard creationist claim that there are no transitional fossils: there are no transitional mutations, either! When we see variations in morphology between populations of organisms, how did those changes get there, were they implanted by angels? As clear examples of “transitional mutations”, I’d point to polyphenisms, cases where there are discrete differences between genetically identical individuals based entirely on their environment.

I also suspect that the poorly explained basis of his question is that lab-generated mutations tend to be changes of very large effect on single genes. Polygenic phenomena are much harder to pick up and harder to analyze, and subtle variations in a fly or a worm are hard for us humans to detect, so the reason we see big, harmful mutations in the lab is because we’re looking for big, harmful mutations.

One more thing: look at sticklebacks. We find gross variations in form, armor, and spines that are caused by tiny changes in gene regulation.

8 ) On your blog, you have defended the central dogmatist (gene-centric) view that an organism’s DNA sequence contains both the necessary and sufficient information needed to actualise an embryo’s final morphology. If your position is so well supported and the position espoused by Jonathan Wells (and others) is so easily refuted, then why do you perpetually misrepresent his views? For example, you state “These experiments emphatically do not demonstrate that DNA does not matter … [Wells’] claim is complete bunk.” Where has Jonathan Wells stated that DNA “does not matter”? Moreover, contrary to your assertions, the phenomenon of genomic equivalence is a substantial challenge to the simplistic “DNA-is-the-whole-show” view espoused by the majority of neo-Darwinists. Cells in the prospective head region of an organism contain the same DNA as cells in the prospective tail region. Yet head cells must turn on different genes from tail cells, and they “know” which genes to turn on because they receive information about their spatial location from outside themselves — and thus, obviously, from outside their DNA. So an essential part of the ontogenetic program cannot be in the organism’s DNA, a fact that conflicts with the DNA-centrism of neo-Darwinism. Some attempts to salvage DNA programs (e.g. Rinn et al.) rely on “target sequences” — molecular zipcodes, if you will — of amino acids that direct proteins to particular locations in the cell. But such “molecular zipcodes” do not create a spatial co-ordinate system, they presuppose it.

This one is totally hilarious. First sentence: he claims I advocate a central dogmatist (gene-centric) view that an organism’s DNA sequence contains both the necessary and sufficient information needed to actualise an embryo’s final morphology, and to support that, links to one of my articles where I supposedly get all totalitarian for dogmatic genecentrism. Go ahead, follow the link. I say exactly the opposite.

10) Why do Darwinists continue to use the supposed circuitous route taken by the vas deferens from the testes as an argument for common descent when, in fact, the route is not circuitous at all? The testes develop from a structure called the genital ridge (the same structure from which the ovaries develop in females, which is in close proximity to where the kidneys develop). The gubernaculum testis serves as a cord which connects the testes to the scrotum. As the fetus grows, the gubernaculum testis does not, and so the testis is pulled downward, eventually through the body wall and into the scrotum. The lengthening vas deferens simply follows. And, moreover, before the vas deferens joins the urethra, there needs to be a place where the seminal vesicle can add its contents.

Wait, what? The route isn’t circuitous? I don’t know about you, but my testicles dangle down right next to my penis, yet the plumbing connecting them has to go back up into my torso, then down and around to exit in just the right place, a few inches away. And yes, there has to be a fluid contribution from the prostate, but again, that organ is tucked away inside, away from the action. And why do the testes have to be dangling anyway? Put ’em up next to the prostate. It would make far more sense.

Sure, you can put together physiological explanations for why each of those organs is in its particular place, but it doesn’t change the fact that the whole assemblage is a contingent kluge stuck together opportunistically.

My talk at Glasgow Skeptics

Hey, it’s on youtube already. There may be a few moments where I look a bit strained — that’s because the video projector wasn’t working well, and we actually had it sitting on the floor kind of crookedly aimed at the screen, and a helpful fellow was maneuvering it to make sure the part I was referring to was on the screen rather than the wall or the ceiling. But fortunately for you, those clever folks who produced the video spliced my slides directly into the video.

It’s all about the real history of Haeckelian recapitulation and why evolution doesn’t predict the crazy stupid things creationists say it does and why Jonathan Wells is a perfidious dorkwad.

Making faces

Faces are weird. They really are largely accidents of development — all the fine features that we consider lovely sculpted signifiers of beauty are really just products of developmental processes, and what we recognize as pretty is actually just a good job of assembly. I’ve been talking about this bizarre way the human face is built for many years, especially since my interest in teratology means I spend a fair bit of time looking at cases where the assembly goes drastically wrong (in fish, not people; I can make things go wrong in fish embryos in ways that would send the mob after me with torches and pitchforks if I did them to human babies). Here’s what your face looked like, once upon a time.

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Drawings of the developing human head and face between the 4th and 5th week (adapted from Nelson, 1953). The top row are side views, and the bottom row are face views of the same stages. The face develops from extensions and fusions of the pharyngeal arches, structures which are found in all other vertebrates, and which are modified in different ways in different species. Abbreviations: m, maxillary process (upper jaw); j, lower jaw; h, hyoid; n, nasal pit.

See what I mean by weird? Embryonically, much of your face was constructed from these plastic bars of tissue called pharyngeal arches, which extend to meet at the midline and then fuse and shift in complicated ways to form the familiar face we see in the mirror.

Now, even better, the BBC has created a simulated time-lapse video of face assembly. There are patent rules to how these tissues move, and common birth defects, like cleft palate, are a consequence of simply understood errors in how these tissues come together in the midline.

The article makes the point that the characteristics of facial development are also relics of our fishy ancestors. I guess it’s a good thing I study these phenomena in fish, after all, in addition to benefit of not enraging the local peasantry.

The basics of building a kidney

I’m a major fan of kidneys — they’re fascinating organs for discussion of both development and evolution. Today I lectured about them in my human physiology course, but I could only briefly touch on their development, and instead had to talk on and on about countercurrent multipliers and juxtamedulary nephrons and transport membranes and all that functional physiology stuff. So I thought I’d get the evo-devo out of my system with a few words about them here.

Our kidneys go through an elaborate series of three major developmental stages — we essentially build three pairs of kidneys as embryos, and jettison two pairs as we go along. It actually looks like something out of Haeckel’s recapitulation theory, as we progressively assemble and then discard ‘primitive’ kidneys.

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The first stage is the formation of the pronephric kidney. In the embryo, the circulatory system forms glomeruli, or tangled capillary beds, adjacent to the membrane that surrounds the body cavity, or coelom. Filtered plasma oozes into the coelom, and the pronephric kidney has ciliated openings into the coelom called nephrostomes, and the fluid is drawn into the tubules, where membrane pumps recover nutrients and salts and return them to the circulatory system. Whatever is left behind — wastes and water — trickles into the pronephric duct, which terminates in the cloaca.

It’s a simple, low pressure system that is adequate for collecting waste products from the early embryo. It relies on an existing cavity for collecting filtered fluids, and you can tell that it doesn’t use a high-pressure filtration scheme since it can get by with simple ciliary beating to cause fluid flow. It’s a primitive system that is retained for functional reasons: metabolizing embryonic cells are producing chemical waste products, and some kind of waste disposal system is essential for even this early stage.

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The second stage is the mesonephric kidney. New tubules bud off the pronephric duct, but unlike the pronephric tubules, these are directly invested with capillary glomeruli and form spherical filtrate collectors called Bowman’s capsules. This is the big functional difference from the pronephros: filtered fluids are no longer collected indirectly from the coelom, but straight from the circulatory system. Some of the mesonephric tubules may retain a connection with the coelom, but this is no longer the sole way to collect filtrate.

The pronephros degenerates completely as the mesonephros takes over its job. As it withers away, the mesonephric tubules continue to use the pronephric duct, which gets renamed: it’s now called either the mesonephric duct, or if you prefer the old school names, the Wolffian duct. Even the mesonephros is doomed, though; it’s an intermediate stage that can cope with the light loads of waste produced by the embryo at this point, but an even more elaborate, more efficient kidney, the metanephros, is also beginning to grow, and it’s going to make the mesonephros superfluous.

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The metanephric kidney, the third and final stage of development (the metanephric kidney is the familiar adult kidney we all possess), buds from the mesonephric duct and forms a unique structure with familiar elements. The new kidney makes branching ducts from a central collecting point, like a spray of flowers; these new ducts look just like mesonephric tubules, with a Bowman’s capsule on the outer, or cortical side of the kidney, and loops descending down into the medulla to generate a concentration gradient of salts used in generating hyperosmotic urine (which is what I talked about in class today, and won’t say anything further here). The subunits are similar to the mesonephric tubules, just arrayed in a different and specific organization for even more effective mechanisms for maintaining salt balance.

This metanephric stage is also complicated by the co-development of the reproductive system. The gonads are differentiating and forming alongside the degenerating mesonephric kidney. In addition, another duct, the Müllerian duct forms in parallel to the Wolffian duct, so now, briefly, we have two pairs of kidneys and two pairs of longitudinal ducts. This is going to be followed by consolidation and change, though, and it’s going to be a sex dependent pattern.

In females, the Wolffian duct is mostly going to degenerate and be lost, along with the mesonephros. The Müllerian duct is going to develop into the fallopian tubes, uterus, cervix, and upper vagina. The only part of the mesonephric duct retained will be the branch connecting the metanephros to the cloaca.

In males, the M&uum;llerian duct degenerates. Yes, it seems incredibly wasteful and pointless: we guys built this parallel duct as embryos, and then promptly threw it away, unused. Instead, the Wolffian/mesonephric duct is retained and becomes the ductus deferens, that useful tube for transporting sperm from the testis to the penis.

I think you can see what’s cool about the kidneys — they follow a sequential pattern of development that also happens to reflect the evolutionary history of kidneys. You might be tempted to speculate that it follows a Haeckelian model, where development necessarily follows an evolutionary trajectory because change can only come by addition of new features, but don’t be fooled. There are a couple of reasons why this peculiar pattern of retaining ancient kidney types is maintained.

One is existence of developmental linkages: disrupting any of these earlier kidneys leads to serious developmental anomalies in subsequent kidneys. Each kidney is built on the foundations of the previous one; mutations that would excise that old less efficient, less sophisticated form would also prevent the normal development of the metanephros. Even if they were totally non-functional, we would still need the patterning aspect of the primitive kidneys to be present.

The other reason is functional. The metanephric kidney is complex and intricate, and takes more time to develop — but cellular metabolism isn’t going to just stop everywhere else in the embryo and wait for the kidneys to be put in place. It’s like the situation when construction workers are building a house, and they still occasionally need to empty their bladders, even if the elaborate bathroom faced with Grecian marble and equipped with the latest German plumbing fixtures isn’t done yet … so a porta-potty is wheeled onto the site.

And that’s what I like about kidneys: all the funky relics of the construction process are still there, hanging out and seeming to contribute to an excessively complex tangle of complicated relationships.


Kalthoff K (2001) Analysis of biological development. McGraw-Hill, NY.

Squid in space

The last mission of the space shuttle will contain a student-initiated experiment: a collection of bobtail squid embryos will be launched into space. Which is cool, I suppose. I like squid, I like space, I like science, I like student research, let’s just throw them all into one big tossed salad of extravagantly expensive tinkering.

So why am I so disappointed?

Because the experiment is so trivial and uninteresting. The squid Euprymna has a commensal relationship with the luminescent bacterium, Vibrio. Early in their development, special organs in the squid are colonized by the bacteria; the squid provides a privileged environment for Vibrio growth, the bacteria give Euprymna a glowing organ that is thought to camouflage itself when viewed from below against a moonlit sky. This is a really cool phenomenon that has engaged the interest of many researchers, and there is serious work being done on the genetics and development of the symbiosis.

But, you know, I’ve never seen any speculation that gravity is a significant factor in the interaction. There’s cilia, and there are secreted amino acids, there is a mucus trap, and there’s a venting process, but gravity? Why would that matter?

I suspect the experiment was chosen because it’s easy for the shuttle engineers and technicians. Load up some chambers with embryos, launch it into space where it will require minimal attention from the crew, assay the results, that is, the development of the light organ, when it returns to earth. The results don’t matter. NASA will check off an item on a list, and say, yep, we did experimental embryology on the shuttle, and we gave a little bit of space to a student research project.

And what will the results be? Most likely, the light organ will be colonized and develop perfectly normally, because there’s no reason to think that microgravity will affect it. Or there will be abnormalities, which could either be because delicate embryos do not take well to the abuse of a shuttle launch, so we’re seeing the effect of stress, or there will be some surprising peculiarity in development that suggests maybe microgravity does make a difference, but repeating and expanding the experiment to puzzle out what’s going on will be out of the question.

I get the impression that NASA is simply filling a quota of interdisciplinary research for PR purposes, with only a nominal investment in the project. I wish I could be more of a cheerleader for the combination of space and developmental biology, but I haven’t yet seen an engaging project that would actually help me understand anything. There’s good science that we do because we really want to find an answer, and there’s lazy science that we do just because we can. This is an example of the latter, I’m sorry to say.

SDB 2011: Posters!

Those of you who’ve been to a poster session at a science meeting know that they’re noisy and chaotic and entirely reliant on interaction to work…so I’m not even going to try and describe it. Instead, I strong-armed Eric Röttinger into describing his poster on video for me, and here it is. He’s describing his work on Kahikai, an online database for collecting information about the development of marine invertebrates.

Paul Nelson takes a stab at Ontogenetic Depth again…which makes me go stab-stab-stabbity-stab

Paul Nelson has deigned to write a two-part essay on “Ontogenetic Depth“, his sciencey made-up term for a metric that he claims makes evolution essentially impossible. We’ve been wrangling over this for a long time — he and Marcus Ross introduced this in a poster at the Developmental Biology meetings in 2004, titled “Understanding the Cambrian Explosion by Estimating Ontogenetic Depth”, and in our conversation at that time I certainly got the impression that he and Ross were busy collecting this peculiar thing alien to creationists called “data”. I have asked him multiple times over the last 7 years how to estimate this hypothetical number; at the meetings, I recall asking him specifically how I would go back into my lab and measure it in my zebrafish. He was evasive. We’ve been trying to get him to explain this datum, which was his pretext for getting into a professional meeting, and gotten nothing.

Well, now we’re done. His first point in his first essay is that “ontogenetic depth” is “A Biological Distance That’s Currently Impossible to Measure”.

Oh.

So what the heck were Paul Nelson and Marcus Ross doing? Nelson was certainly doing his best to pretend that they were actually doing real work on this metric, but I should have known better: a failed young-earth creationist philosopher could not possibly have been soiling his hands with empiricism. Now he’s frantically arguing that it doesn’t matter, that once upon a time no one knew the distance from the earth and the sun, but they could at least name the concept, so he can take credit for at least recognizing a real problem, and he can also patronizingly thank me for pointing out that they don’t actually have the tools right now to actually measure it.

Wait, how can they thank me for that? I’m picturing Nelson and Ross sitting at a microscope and looking at eggs of a nematode or a zebrafish or a frog, rubbing their hands in anticipation of a productive morning, and then staring at each other and wondering what to do next…and end up inventing a term for something that they don’t know how to measure. And then a year or so later, Nelson encounters me, I peevishly tell him that he doesn’t know how to measure cell division and differentiation in terms of a single numeric metric, and seven years after that, Nelson finally slaps his forehead and admits “Hey, we don’t know how to measure that!”

I don’t want credit for pointing out the obvious to the clueless, especially not when they’re that slow.

His first essay is an exercise in rationalizing away how he could propose this obstacle to evolution while not having the slightest idea how to measure it. His second essay is an exercise in demonstrating that he doesn’t understand basic biology. He has gussied it up with brightly colored diagrams of cell pedigrees that he purports illustrate the problem, but I think are actually more intended to distract and confuse and make you think he’s actually thought deeply about the subject.

Here’s the gist of his conceptual difficulty: he can’t imagine how the first metazoan got from a crude colonial state, where it’s just a mass of identical cells clumped together, to a state in which regions are consistently specialized for specific functional roles, with the simplest example of an animal that contains only two cell types, a mass of somatic cells that take care of feeding and motility, and a smaller mass of germ cells that do the job of reproduction. Why, that would require a whole series of mutations that selection can’t possibly explain! How could selection possibly create a cell that contains a series of instructions to build a cell type that isn’t going to reproduce?

I’m wishing that Nelson hadn’t chosen to focus on biology. If only he were a creationist philosopher of physics, he’d be the one asking, “magnets, how do they work?” and somebody else would get the job of correcting him.

Nelson summarizes the problem as, at the minimum in the simplest possible metazoan, a three step sequence. First, cells have to divide and stick together; second, they have to have a way to make daughter cells differ from one another; and third, there has to be inheritance of that differentiated state in sublineages. He claims that in none of these steps can selection be involved; this complex process had to evolve independently of any selective effects.

That’s nonsense. The first metazoan already had all the tools needed to build these steps, honed by a billion years or more of selection in single-celled organisms. All three of his steps are found in bacteria.

Step one is simply cell adhesion. Step two is gene regulation. Step three is epigenetics. That’s it. These aren’t glorious novelties invented by the first animals, they inherited this toolkit from their ancestors. Bacteria have been sticking together for billions of years, and they’ve been responding to their local environment by shifting patterns of gene expression for just as long. A bacterium in a sugar-rich environment vs. a bacterium in a sugar-poor environment will make long term changes in gene activity that can persist for a few generations using exactly the same mechanisms as an animal embryo sets up germ and somatic tissues; has Nelson never heard of Jacob and Monod?

Nelson’s argument goes beyond pure ignorance, however. He also recruits Lewis Wolpert to his side, which is remarkable. Wolpert is a brilliant and influential developmental biologist who shaped many of our ideas about differentiation, pattern formation, and evolution. He cites Wolpert as postulating as serious problems for evolution the origin of the egg, and in particular implying that Wolpert sees metazoan evolution as violating a principle. Here’s what Nelson says about a particular paper Wolpert wrote.

Evolutionary developmental biologist Lewis Wolpert — whom no one, even in his wildest delirium, would ever mistake for an ID theorist — had long critiqued the scenario on functional grounds, using what he called “the continuity principle.” (1994) The continuity principle requires that any change occurring in an evolutionary transformation be biologically possible, that is, viable and stably heritable in the next generation.

Whoa — eminent anti-creationist scientist critiques an evolutionary explanation! I’m sure this must make you wonder, familiar as you are with creationist tactics, what Wolpert actually said. Judge for yourself, here’s the abstract for Wolpert’s paper, does it sound like he’s on Nelson’s side at all?

A scenario for the evolution of a simple spherical multicellular organism from a single eukaryotic cell is proposed. Its evolution is based on environmentally induced alterations in the cell cycle, which then, by the Baldwin effect, become autonomous. Further patterning of this primitive organism–a Blastaea, could again involve environmentally induced signals like contact with the substratum, which could then become autonomous, by, perhaps, cytoplasmic localization and asymmetric cell division. Generating differences between cells based on positional information is probably very primitive, and is well conserved; its relation to asymmetric cell division is still unclear. Differentiation of new cell types can arise from non equivalence and gene duplication. Periodicity also evolved very early on. The origin of gastrulation may be related to mechanisms of feeding. The embryo may be evolutionarily privileged and this may facilitate the evolution of novel forms. Larvae are secondarily derived and direct development is the primitive condition as required by the continuity principle.

This is a paper in which Wolpert explains how multicellularity could have evolved, directly answering the questions Nelson raised with his supposedly problematic three steps. How did Paul Nelson miss that?

But wait! There’s more Wolpert abuse!

Nelson has found a paper by Wolpert in which he points out a serious problem in a particular evolutionary strategy, and Nelson, apparently primed by a selective reading of science papers for the magic words “problem”, “difficulty”, “impossible”, or “unlikely” has seized upon it as another instance of Eminent Scientist Critiquing Evolution.

What mechanism is coordinating gene expression among all the members of the colony, such that only one cell lineage will evolve to carry the complete instruction set required to specify the form of the whole? How are mutations — occurring in all individual cells of the colony — transmitted to the next generation? If individual cells continue to reproduce via normal fission, or budding, notes Wolpert, “cell lineages [will be] mutating in all sorts of directions in genetic space.” (2002, 745) Given such genetic chaos, he argues, “we consider it practically impossible” for the collection of cells to “yet retain the ability to evolve into viable new forms.”

Sounds dreadful. I give up, I guess evolution must actually be impossible.

Hang on, though, maybe we should read Wolpert’s paper first. And there what you discover is a story that you would not have expected from Nelson’s peculiarly distorted coverage. It’s a short paper where the authors consider alternative reproduction strategies: not all animals go through a single-cell stage in reproduction, you know. Some, like hydra, reproduce by budding, where a small collection of cells, not just one egg or sperm cell, splits off to form an independent organism. Wolpert is considering which solution is more advantageous for evolution, going through a single-cell bottleneck or through a larger population that would reduce the dangers of mutations? And that’s where Wolpert’s criticisms lie: the asexual budding solution is the focus of his critique, and which is where Nelson draws his quotes highlighting the difficulty of evolution.

In a hydra-like organism that only reproduces by asexual budding, it is impossible to evolve significant changes. There is no way that the genes in the huge number of cells involved in budding can change at the same time, and mutations in individual cells mean that they no longer share the behavioural rules of the majority. It is only through a coherent developmental programme, with all cells possessing the same genes, that organisms can evolve, and this requires an egg.

Huh. So Wolpert is arguing that development from a multicellular propagule is much less evolutionarily flexible than evolution from a single-celled egg. His thesis is explaining why we develop from eggs, not that our evolution is unlikely.

We consider it practically impossible to have many asexual, differentiated cell lineages mutating in all sorts of directions in genetic space and yet retain the ability to evolve into viable new forms. This may not be completely impossible but, taking the broad view in evolutionary terms, organisms that develop from an egg would displace those that do not.

Dang, Paul Nelson. You should be smart enough to know that you don’t quotemine claims from the science literature in an argument with someone who has actually read that literature.

Clarifying tetrapod embryogenesis, accurately

Clarifying tetrapod embryogenesis, accurately
By OldCola

[Note from pzm: The text of this one is a little rougher than I like, but the content is interesting and addresses the claims of a character who has been lurking about here for a while, and whose work I’ve criticized before. If nothing else, I’d also like to see a few science posts submitted as guest articles, so think of this as priming the pump.]

The article, “Clarifying tetrapod embryogenesis, a physicistʼs point of view,” by V. Fleury, hasn’t steered the revolution expected by Fleury in evo-devo. Two years after the publication, cited by one (Fleury himself), the article seems to have being more useful to clarify the way he perceives the world, then anything related to the tetrapods embryogenesis. And the most useful elements are to be found on the Web, not in the article per se. Direct questions remain unanswered, critics are threatened by legal action for defamation, and hierarchical superiors are solicited to politely ask the critics to STFU.

While Fleury must be aware by now of major flaws in the way he represented several of the articles he used as sources of information, and of several inconsistencies of his model and the way he extrapolates his own data, he doesn’t seem to have done anything to correct them. The article remains available unchanged, a shame for EPJ AP editorial board (and Editor-in-Chief Dr Drévillon B. in particular), sufficiently shameful at least for the guy who invited the review, for Fleury to avoid disclosing his name.

A new element comes to complete Fleury’s quest:

The pattern of tetrapods exist in the platonician space of forms, just like the sphere. You can write its essence without evolutionnary arguments.

V. Fleury, Dynamic topology of the cephalochordate to amniote morphological transition: A self- organized system of Russian dolls, C. R. Biologies (2011), doi:10.1016/j.crvi.2010.11.009

During evolution of vertebrates a sequence of events is empirically observed: first, animals are bilateral, but they have no heart, no head, and no surrounding bag during development (these primitive animals are called cephalochordates [1]).


From the very first phrase of the Introduction, you know hope that no biologist read the manuscript before it was accepted for publication. And certainly not any evo-devo person, which would be the right choice for a referee for this kind of subject.

Cephalochordates are certainly not vertebrates and they certainly have a head, the sub-phylum being named after the fact that the notochord extends into that head. One may think that Fleury misused the word “head”, meaning “skull” or whatever, but if you read the French summary of the paper you do get the same information, Cephalochordata don’t have a “tête” (French for “head”).

And he dare give a reference! But if you had the courage to read his previous article (for a review) you may be familiar with the strange way Fleury reports his readings (at least the way he understood them), in an absolutely surreal way, including data from his own lab! If not, there is a brand new example in this one (see below).

By the title you may have expected to read about comparative embryology/anatomy that will enlighten you on the relations between the body plans of cephalochordates and amniotes. If so, you will be deceived. Fleury focuses entirely on chicken embryos, hoping to prove experimentally the existence of some kind of order in the ontogeny of the chicken that reflects an order in the phylogeny of chordates. The reading is interesting not to learn anything about evolution or embryology (or physics by the way), but to see how an a priori can lead someone to mess up things badly. Fleury observes the world through a keyhole shaped by Plato a long time ago and he seeks some equivalent of the Holly Grail: a way to write the essence of the pattern of tetrapods without evolutionary arguments, as it “exist in the platonician space of forms, while avoiding being embarrassed by the bullshit produced by embryologists, geneticists or evo-devo people.

The aim of this work is to support that “the formation of amniotes would be a deterministic attractor of a physical process over a flat visco-elastic plane,” and that the formation of the heart and the chorion (you should pronounce it amnios to make sense) are the consequence of the body’s growth along the anteroposterior axis.

Thus, any embryo with the amniotic (and chorionic) cavity formed before the beginning of gastrulation would falsify Fleury’s model definitively. I’ll come to that later.

While aware of the lateral folding of the embryo around an antero-posterior (AP) axis, Fleury avoid to discuss it as his model don’t explain it. Cardiac tubes are formed as mirror structures at both sides of and parallel to the AP axis, they migrate to the midline where they fuse to form the heart and they are already pre-determined to produce almost fully developed hearts if by some mutation their migration to the midline is impaired. Cardiac formation is not caused by the the cephalic fold renamed “cardiac fold” by Fleury.

The fact that the cephalic and caudal folds forming the anterior and posterior intestinal portals are distant in time by almost 24 h doesn’t bother him and his model lack any modality that would explain the latency for the formation of the posterior intestinal portal. On the contrary, he manage to represent the two folds as the result of the AP axis extension in a single schema, as being the consequences of a single phenomenon, “[f]or the sake of clarity“. He is not at his first temporal jump of embryonic structures, even of imaginary ones.
What kind of physicist could have reviewed the manuscript without requiring some kind of explanation about this particularity?

There is nothing really new in his description of the development of the chicken embryo, except the errors and omissions which make it unusable. One may prefer a classic textbook, published a while ago: Patten, B.M. (1920). The Early Embryology of the Chick. Philadelphia: P. Blakiston’s Son and Co. You can browse through it at UNSW Embryology pages, where the scans of the illustrations are of much better quality.

Some data may be interesting for people interested by the dynamics of the embryo formation, the article being based on time lapse videos of the developing embryo. There is no much of it and the graphics seem to report on single experiments (no number of observed embryos given, no variance bars on the graphics). What is really new for me, is that Fleury found a way to report a “rate of variation of the radius” of an ellipse, with a major vs minor axis ratio of ~1,5 (fig 3, a, 0′), giving a single value! Any mathematician around to explain us this?

As Fleury decided to rename the formation of the subcephalic pocket “cardiac fold”, and he was seeking some symmetry at the caudal region, he also renamed the subcaudal pocket “cardiac fold” and he triumphantly mention the “aneural heart” of the hagfish as an evidence of the power of prediction of his model. Now, the caudal heart of the hagfish is just a pair of specialized structures on the caudal veins, parallel to the AP axis, as the primitive heart tubes, separated by a cartilage septum and they are innervated! Jensen, in the Introduction of his paper clearly explain the anatomy of the circulatory system of the hagfish and what elements are innervated, or not. Either Fleury didn’t bothered reading the paper or he is simply unable to understand what he is reading (or both, your guess). It would have be nice if he had read the paper, because he passed over the existence of the portal heart and of what some people call the cephalic hearts of the hagfish (specialized gill musculature which propel the blood through the arterial circulation). There is even an illustration for people bored by textual explications (fig 4). Such a little animal, so many hearts and not enough folds to explain them. Unnerving.

Patten starts his Introduction by a very wise advice:

The only method of attaining a comprehensive understanding of embryological processes is through the study and comparison of development in various animals.

As I said, any embryo with the amniotic cavity formed before the beginning of gastrulation would falsify Fleury’s model definitively. Let me present you an artist’s rendition of Dr Fleury at his early youth, second week of development

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The illustration is from the online Human Embryology course notes (clic the image for the full page). I’m not sure they had in mind Vincent Fleury when they draw this cartoon, but it’s the best I can offer you: A cute embryo with his amniotic cavity lined with cells from the epiblast and his primary yolk sac lined by cells derived by the hypoblast. The Heuser’s membrane is still attached to the extraembryonic reticulum.
A few days later, the secondary yolk sac had formed and the chorionic cavity was installed.

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At this stage little Vincent was still bilaminar with fully formed amniotic and chorinic cavities.

Those of you interested to learn about embryo’s folding can also visit Folding of the germinal disk and the generation of the abdominal wall, in which case the comparison of the two foldings (cephalo-caudal and lateral), animation is a must for the visitor, and certainly for Fleury.

How sad that a great model from an experimentalist working all day with embryos, goes down the drain after being confronted to elements of chapter 5 of a Human Embryology textbook.

Several questions come in mind in this situation, the first one being: who the hell reviewed the manuscript. Not a biologist, probably not a physicist (he should have ask for a mechanism explaining the delay of formation of the caudal fold). Not a second year student of biology or medicine neither; she would have spotted the problem with the amniotic and chorionic cavities subito presto.
Fleury’s precedent paper was an invited review by one of the editors of a journal of physics. You can’t blame the guy for being unable to understand the bunch of errors the review contains. OK, you can blame him for not having a specialist’s opinion on the final piece of work. Misplaced trust. And sometimes, some physicists are just pissed-off by life scientists. Fleury didn’t even dared to give his name.

This time, the journal is a publication of the French National Academy of Science and it displays “Biologies” on the cover. Shame on them. Until this paper is retracted who would trust the “Development and reproduction biology” section of the journal, or the journal at all? I wouldn’t, would you?

Therefore, this suggest” is one fabulous transition.

The Methods section of the paper may be interesting if you plan a few experiments with chicken embryos, but dramatically incomplete. The most interesting part is missing: the references of the software and the method Fleury is using for PIV, which gives him astonishing images. I would like to be able to check by myself, previous interpretations of experimental data, even the ones generated in his lab, by Fleury being as much surreal as his usual stuff. Hopefully he could complete this section in the comments of this post.

In Heart formation, Fleury undergo to explain how the heart is formed by the heart fold. Here is the first part where it goes really bad. I can understand the frustration of a physicist who would like to have more data concerning the biomechanics of the process, and hopefully somebody else than Fleury will go for them. But there is no need to reinvent the wheel, there are nice descriptions of the movements by which the heart tubes are forming, how the lateral folding of the embryo make them join along the anteroposterior axis and describing their fusion to produce the unique heart tube [1]. Certainly, the 125° rotation of the heart fields and the lateral folding of the embryo necessary for the normal cardiogenenic process are not perpendicular to the anteroposterior axis and doesn’t fit Fleury’s model, but it isn’t reasonable to just ignore them. You can’t just ignore what it doesn’t fit your model to make it sound plausible.
Anyway, even the fusion of the primary heart tubes doesn’t seem to be necessary to support the development and morphogenesis of the heart, up to some point: “a highly differentiated four-chambered mammalian heart” in the case of Foxp4 mutant mice embryos [2].

The point of junction of the cardiac tubes do travel caudaly along the anteroposterior axis of the embryo, but that’s just the point of junction…

An interesting description of the heart formation can be found in a relatively old textbook: The Early Embryology of the Chick (pp 68-72, fig. 26 & 27, with emphasis for fig 27) [3]

For those who will take the time to read the paper, please pay attention to the part discussing the role of chemotactic forces ; Fleury didn’t managed yet to understand morphogenic gradients and that most of them are embedded into the cells and the extracellular matrix.

You may need to go through the whole section about the Chorion formation to understand that Fleury discuss just about the amniotic folds of the chorion and completely ignores the rest of it. It’s just that it isn’t folded in the right direction for his model. On the other hand the amniotic folds of the chorion are folded in the right way and Fleury carefully studied the ways the meet around a single point. Not only it’s weird how he doesn’t discuss the lateral part of the amniotic folds (absolutely necessary to form the amnios and the dorsal part of the chorion), but not perpendicular to the anteroposterior axis, but somehow he manage to found a single rate of variation of the radius of an ellipse!

Patten [3] offers a series of diagrams showing the growth and foldings of the somatopleure which form the amnios, from transverse sections of the embryo, in fig 30 and from longitudinal sections in fig. 32. That gives a global image of the tissue growth, in all directions, not just the keyhole presentation Fleury is giving in his article.

While Fleury is aware that the cephalic and caudal amniotic folds appear at different developmental stages, he present their occurrence as being caused by the “extension of the median axis” without explaining what may be the mechanical causes for the delay of almost 24h for the apparition of the caudal amniotic fold. “For the sake of clarity” he present them in the same figure (4b of his paper) as if they occurred in the same time. As much clarity as usually.


1. Heart Field: From Mesoderm to Heart Tube, Radwan Abu-Issa, and Margaret L. Kirby, Annual Review of Cell and Developmental Biology Vol. 23 (2007): 45-68, doi: 10.1146/annurev.cellbio.23.090506.123331

2. Advanced Cardiac Morphogenesis Does Not Require Heart Tube Fusion, Shanru Li, Deying Zhou, Min Min Lu, Edward E. Morrisey, Science Vol 305 (2004): 1619-1622, doi: 10.1126/science.1098674
3. Patten, B.M. (1920). The Early Embryology of the Chick [link to scans in pdf at archive.org]. Philadelphia: P. Blakiston’s Son and Co. You can browse through it at UNSW Embryology pages, where the scans of the illustrations are of much better quality.


V. Fleury, Dynamic topology of the cephalochordate to amniote morphological transition: A self-organized system of Russian dolls, C. R. Biologies (2011), doi:10.1016/j.crvi.2010.11.009

Will radiation hormesis protect us from exploding nuclear reactors?

That reputable scientist, Ann Coulter, recently wrote a genuinely irresponsible and dishonest column on radiation hormesis. She claims we shouldn’t worry about the damaged Japanese reactors because they’ll make the locals healthier!

With the terrible earthquake and resulting tsunami that have devastated Japan, the only good news is that anyone exposed to excess radiation from the nuclear power plants is now probably much less likely to get cancer.

This only seems counterintuitive because of media hysteria for the past 20 years trying to convince Americans that radiation at any dose is bad. There is, however, burgeoning evidence that excess radiation operates as a sort of cancer vaccine.

As The New York Times science section reported in 2001, an increasing number of scientists believe that at some level — much higher than the minimums set by the U.S. government — radiation is good for you.

But wait! If that isn’t enough stupid for you, she went on the O’Reilly show to argue about it. Yes! Coulter and O’Reilly, arguing over science. America really has become an idiocracy.

I only know about hormesis from my dabbling in teratology; a pharmacologist or toxicologist would be a far better source. But I know enough about hormesis to tell you that she’s wrong. She has taken a tiny grain of truth and mangled it to make an entirely fallacious argument.

Radiation is always harmful — it breaks DNA, for instance, and can produce free radicals that damage cells. You want to minimize exposure as much as possible, all right? However, your cells also have repair and protective mechanisms that they can switch on or up-regulate and produce a positive effect. So: radiation is bad for you, cellular defense mechanisms are good for you.

Hormesis refers to a biphasic dose response curve. That is, when exposed to a toxic agent at very low doses, you may observe an initial reduction in deleterious effects; as the dose is increased, you begin to see a dose-dependent increase in the effects. The most likely mechanism is an upregulation of cellular defenses that overcompensates for the damage the agent is doing. This is real (I told you there’s a grain of truth to what she wrote), and it’s been observed in multiple situations. I can even give an example from my own work.

Alcohol is a teratogenic substance — it causes severe deformities in zebrafish embryos at high doses and prolonged exposure, on the order of several percent for several hours. I’ve done concentration series, where we give sets of embryos exposures at increasing concentrations, and we get a nice linear curve out of it: more alcohol leads to increasing frequency and severity of midline and branchial arch defects. With one exception: at low concentrations of about 0.5% alcohol, the treated embryos actually have reduced mortality rates relative to the controls, and no developmental anomalies.

If Ann Coulter got her hands on that work, she’d probably be arguing that pregnant women ought to run out and party all night.

We think there is probably a combination of factors going on. One is that alcohol is actually a fuel, so what they’re getting is a little extra dose of energy; it’s also deleterious to pathogens, so we’re probably killing off bacteria that might otherwise harm the embryos, and we’re killing those faster than we are killing healthy embryonic cells. It’s the same principle behind medieval beer and wine drinking — it was healthier than the water because the alcohol killed the germs.

However, the key thing to note about hormetic effects is that they only apply at low dosages. Low dosages tend to be where the damaging effects are weakest, anyway, and where the data are also the poorest. The US government recommendations for radiation exposure are based on a linear no threshold model in which there is no hormesis to reduced effects at low concentrations for a couple of reasons. One is methodological. The data we can get from high exposures to toxic agents tends to be much more robust and consistent, and we do see simple relationships like a ten-fold increase in dose produces a ten-fold increase in effect, whereas at low doses, where the effects are much weaker, variability adds so much noise to the measurements that it may be difficult to get a repeatable and consistent relationship. So the strategy is to determine the relationships at high doses and extrapolate backwards.

Then, of course, the major reason recommendations are made on the simple linear model is that it is the most conservative model. The data are weaker at the low end; there is more variability from individual to individual; the safest bet is always to recommend lower exposures than are known to be harmful.

In the low dosage regime, these responses get complicated at the same time the data gets harder to collect. This is why it’s a bad idea to base public policy on the weakest information. I’ll quote a chunk from a review by Calabrese (2008) that describes why you have to be careful in interpreting these data.

In 2002, Calabrese and Baldwin published a paper entitled “Defining hormesis” in which they argued that hormesis is a dose-response relationship with specific quantitative and temporal characteristics. It was further argued that the concept of benefit or harm should be decoupled from that definition. To fail to do so has the potential of politicizing the scientific evaluation of the dose-response relationship, especially in the area of risk assessment. Calabrese and Baldwin also recognized that benefit or harm had the distinct potential to be seen from specific points of view. For example, in a highly heterogeneous population with considerable inter-individual variation, a beneficial dose for one subgroup may be a harmful dose for another subgroup. In addition, it is now known that low doses of antiviral, antibacterial, and antitumor drugs can enhance the growth of these potentially harmful agents (i.e., viruses), cells, and organisms while possibly harming the human patient receiving the drug. In such cases, a low concentration of these agents may be hormetic for the disease-causing organisms but harmful to people. In many assessments of immune responses, it was determined that approximately 80% of the reported hormetic responses that were assessed with respect to clinical implications were thought to be beneficial to humans. This suggested, however, that approximately 20% of the hormetic-like low-dose stimulatory responses may be potentially adverse. Most antianxiety drugs at low doses display hormetic dose-response relationships, thereby showing beneficial responses to animal models and human subjects. Some antianxiety drugs enhance anxiety in the low-dose stimulatory zone while decreasing anxiety at higher inhibitory doses. In these two cases, the hormetic stimulation is either decreasing or increasing anxiety, depending on the agent and the animal model]. Thus, the concepts of beneficial or harmful are important to apply to dose-response relationships and need to be seen within a broad biological, clinical, and societal context. The dose-response relationship itself, however, should be seen in a manner that is distinct from these necessary and yet subsequent applications.

I know, the Cabrese quote may have been a little dense for most. Let me give you another real world example with which I’m familiar, and you probably are, too.

Here in Minnesota in the winter we get very snowy, icy conditions. If I’m driving down the road and I sense a slippery patch, what I will immediately do is become more alert, slow down, and drive more carefully — I will effectively reduce my risk of an accident on that road because I detected ice. This does not in any way imply that ice reduces traffic accidents. Again, with the way Ann Coulter’s mind works, she’d argue that what we ought to do to encourage more responsible driving is to send trucks out before a storm to hose the roads down with water instead of salt.

Ann Coulter is blithely ignoring competent scientists’ informed recommendations to promote a dangerous complacency in the face of a radiation hazard. She’s using a childish, lazy interpretation of a complex phenomenon to tell people lies.


Calabrese EJ (2008) Hormesis: Why it is important to toxicology and toxicologists. Environmental Toxicology and Chemistry 27(7):1451-1474.

Brachiopods: another piece in the puzzle of eye evolution

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About 600 million years ago, or a little more, there was a population of small wormlike creatures that were the forebears of all modern bilaterian animals. They were small, soft-bodied, and simple, not much more than a jellyfish in structure, and they lived by crawling sluglike over the soft muck of the sea bottom. We have no fossils of them, and no direct picture of their form, but we know a surprising amount about them because we can infer the nature of their genes.

These animals would have been the predecessors of flies and squid, cats and starfish, and what we can do is look at the genes that these diverse modern animals have, and those that are held in common we all inherited together from that distant ancestor. So we know that flies and cats both have hearts that are initiated in early development by the same genes, nkx2.5 and tinman, and infer that our common ancestor had a heart induced by those genes…and that it was only a simple muscular tube. We know that modern animals all have a body plan demarcated by expression of Hox genes, containing muscles expressing myoD, so it’s reasonable to deduce that our last common ancestor had a muscular and longitudinally patterned body. And all of us have anterior eyes demarcated by early expression of pax6, as did our ancient many-times-great grandparent worm.

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We do not have fossils of these small, soft organisms, but that’s no obstacle to picturing them. You just have to see the world like a modern molecular or developmental biologist. One of the graphical conceits of the Matrix movies was that the hero could see the hidden mathematical structure of the world, which was visualized as green streams of symbols flowing over everything. We aspire to the same understanding of the structure of life, only what we see are patterns of genetic circuity, shared modules that are whirring away throughout development to produce the forms we see with our eyes; and also, unfortunately, we currently only see these patterns spottily and murkily. There is no developmental biologist with the power of Neo yet, but give us a few decades.

There’s another thing we know about these ancient ancestors: they had two kinds of eyes. ciliary and rhabomeric. Your eyes contain ciliary photoreceptors; they have a particular cellular structure, and they use a recognizable form of opsin. A squid has a distinctly different kind of photoreceptor, called rhabdomeric, with a different cell structure and a different form of opsin. We humans also have some rhabdomeric receptors tucked away in our retinas, while invertebrates have ciliary receptors as well, so we know the common ancestor had both.

Now this ancestral population eventually split into two great tribes, the protostomes, which includes squid and flies, and the deuterostomes, which includes cats and starfish. It should be an obvious indication of the general state of that ancestor that it represents all that those four diverse animals have in common. It also tells us that while that ancestor had eyes, they were almost certainly very simple, and could have been nothing more than a patch of light-sensitive cells, or perhaps even single cells, as we see in some larval eyes.

What we think happened at this division is that both tribes took the primitive eyes and specialized them independently. Each group evolved under similar constraints: they needed directionally-sensitive eyes that could tell what direction a source of illumination was coming from (and these would eventually form true image-forming eyes), and they also needed sensors to detect general light levels — is it day or night, are we in the open or under a rock? Think of it like a camera system: there is a part that gets all the attention, the lens and image-forming chip, but there’s also a light meter that senses ambient light levels.

The two tribes made different choices, though. The protostomes pulled the rhabdomeric photoreceptor out of their toolbox, and used that to make the camera; they used the ciliary photoreceptor to make their light meter. The deuterostomes (actually, just us chordates) instead used the ciliary photoreceptor for their camera, and the rhabdomeric photoreceptor for the light meter. It’s the same ancestral toolkit, but we’ve just specialized in different ways.

At least, that’s the general model we’ve been exploring. A new discovery at the Kewalo Marine Laboratory, one of the premiere labs for evo-devo research, has made the interpretation a little more complex.

That discovery is that brachiopod larvae, which are protostomes, have been found to have directionally sensitive eyes…which are ciliary. A protostome should have directionally sensitive eyes that are rhabdomeric. How interesting!

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Brightfield microscopy of a Terebratalia transversa larva, with red eye spots visible in the apical lobe (black arrows). (A) Dorsal view. (B) Lateral view.

In addition to being ciliary in structure, these eyes express ciliary opsin. They are also true cerebral eyes, also expressing pax6 and having a nervous connection to the central nervous system.

Notice what is going on here: a protostome is building a camera, and unlike all the other protostomes we’ve observed, it’s pulled a ciliary photoreceptor out of its pocket to make it. This is a surprise, but it doesn’t upset any theories too much — it just means we need to explore a couple of alternative explanations. We don’t have answers to resolve these hypotheses yet — we need more data and experiments — but it’ll be fun to watch the work roll onward.

One explanation is illustrated in A, below. The initial animal state was to build directional, cerebral eyes using rhabdomeric photoreceptors. The vertebrates are oddballs who swapped in ciliary receptors instead, while these larval eyes in brachiopods are major peculiarities, an evolutionary novelty which resembles a cerebral eye, but is actually non-homologous. This seems unlikely to me; there are multiple elements of the eye circuitry at work in these eyes, and if they’re using the same gene circuitry, we ought to recognize them as homologous at the molecular level…the only one that counts.

The second explanation in B is that all of these cerebral eyes are homologous, but that the receptor type is more plastic than we thought — it’s relatively easy to switch on the ciliary module vs. the rhabodmeric module, so we would expect to see multiple flip-flops in the evolutionary record.

If we accept that it’s easy to switch receptor type, though, then why assume that the last common ancestor had a directional, cerebral eye that was rhabdomeric? It could have been ciliary, which is also a more parsimonious explanation, because it requires only one switch of types in the protostomes, shown in C.

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(Click for larger image)

Alternative hypothesis on the evolution of photoreceptor deployment in cerebral eyes. Schematic representation of three hypotheses accounting for the deployment of ciliary photoreceptors in the cerebral eyes of Terebratalia and vertebrates, versus rhabdomeric photoreceptors in Platynereis and other protostomes. (A) Deployment of rhabdomeric photoreceptors as the ancestral state in cerebral eyes, with the larval eyes of Terebratalia, containing ciliary photoreceptors, representing an evolutionary novelty. The deployment of ciliary photoreceptors is the result of a substitution (with ciliary photoreceptors having replaced rhabdomeric photoreceptors in the cerebral eyes) early in the chordate lineage. (B) Larval eyes in Terebratalia are homologous to the cerebral eyes in other protostomes, but ciliary photoreceptors have been substituted for rhabdomeric photoreceptors, as in the vertebrates. (C) Ciliary photoreceptors in cerebral eyes represent the ancestral condition, inherited by Terebratalia and vertebrates. Deployment of rhabdomeric photoreceptors in the cerebral eyes of Platynereis and other protostomes are the result of substitution events.

Whichever hypothesis pans out, though, the important message is that photoreceptor type is a more evolutionarily labile choice than previously thought. What I want to see is more research into photoreceptor development in more exotic invertebrates — that’s where we’ll learn more about our evolutionary history.


I have to mention a couple of other cool features of this paper. If you ever want to see a minimalist directional eye, here it is: the larval eye sensor of brachiopods consists of two cells, a lens cell that actually does the job of light detection, and a pigment cell that acts as a shade, preventing light from one direction from striking the lens cell. That’s all it takes.

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I lied! That isn’t a minimal directional eye at all: here it is.

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This rather blew my mind. The brachiopod gastrula senses light. The figure above is of a very early stage in development, when the organism is little more than a couple of sheets of cells with no organs at all, only tisses in the process of forming up into rough structures. It definitely has no brain, no nervous tissue at all, and no eyes…and there it is, that dark blue smear is a region selectively expressing ciliary opsin as if it were a retina. Furthermore, when tested behaviorally (mind blown again…behavior, in a gastrula), populations in a light box show a statistical tendency to drift into the light. Presumably, light stimulation of the opsin is coupled to the activity of cilia used for motility in the outer epithelium of the embryo.

Amazing. It suggests how eyes evolved in multicellular organisms, as well — initially, it was just localized general expression of light-sensitive molecules coupled directly to motors in the skin, no brain required.


Passamaneck Y, Furchheim N, Hejnol A, Martindale MQ, Lüter C (2011) Ciliary photoreceptors in the cerebral eyes of a protostome larva. EvoDevo, 2:6.