Islamic embryology: overblown balderdash

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.

Tzortzis bloats this scrap into a long, tedious potboiler by doing a phrase by phrase analysis, and by comparing it to the work of Aristotle and Galen, who got lots of things wrong. How, he wonders many times, could Mohammed have written down only the correct parts of the Greek and Roman embryological tradition, and avoided their errors, if he weren’t divinely inspired? My answer is easy: because Mohammed only made a vague and fleeting reference to the science of the time, boiling down Aristotle’s key concept of an epigenetic transformation into a few non-specific lines of poetry. Aristotle and Galen got a lot wrong because they tried to be specific and wrote whole books on the subject; you can read the entirety of Aristotle’s On the Generation of Animals. Galen was prolific and left us about 20,000 pages on physiology and medicine.

So, yes, you can find lots of examples in their work where they got the biology completely wrong, and it’s harder to do that in the Quran…because the Quran contains negligible embryological content, and what there is is so sketchy and hazy that it allows his defenders to make spectacular leaps of interpretation. Mohammed avoided the trap of being caught in an overt error here by blathering generalized bullshit, and saying next to nothing. This is neither an accomplishment nor a miracle.

I’ll go through his argument piece by piece, but at nowhere near the length. It’s hard to believe anyone is using this feeble fragment to claim proof of divinity, but then, Christians do exactly the same thing.

  1. “essence of clay”. Tzortzis happily announces that clay contains “Oxygen, Carbon, Hydrogen, Nitrogen, Calcium, Phosphorus, Potassium, Sulfur, Chlorine, Sodium, Magnesium and Silicon; all of which are required for human functioning and development”. These are irrelevant factlets. Clay is a fine-grained hydrous aluminum phyllosilicate; carbon, which is the element to consider in organic chemistry, is present as a contaminant, but the primary elements are aluminum and silicon. It’s nothing like the composition of the human body. This part of Tzortzis case is simply a lie.

  2. “drop of fluid”. Tzortzis tells us that the Arabic word here is “nutfah”, which has a number of meanings, but he likes the interpretation that it implies mingled fluids. Then he babbles on about oocytes and spermatazoa and secretions of the oviduct, none of which are mentioned in the Quran and are completely irrelevant. Bottom line: Arabs noticed long ago that sex involves a mingling of fluids. Brilliant. I think most of us could figure that out without divine inspiration.

    He spends a fair amount of time pointing out that both Aristotle and Galen had a male-centric view of procreation, where the man’s contribution was the dynamic agent and the woman was a passive vessel. They were wrong. In order to rescue the Quran, though, Tzortzis has to bring in Ibn Qayyim, a 13th century Islamic scholar, who pointed out that women have to provide a significant contribution to inheritance, since their traits are also present in the children. This, again, is an obvious and observable property, and the Greeks also argued over the relative contributions of male and female. There is nothing in the Quran that is beyond casual observation or non-existent in the scholarly works of the time.

  3. “in a safe place”. Tzortzis quotes modern embryologists and throws around the terms endometrium, syntrophoblast, implantation, uterine mucosa, proteolytic enzymes, etc., etc., etc. I ask you, is any of that in the quoted verse from the Quran? No. Total bullshit from the apologists. That the embryo grows in a “safe place” — the woman’s belly — is another obvious property.

  4. “a clinging form”. It seems that the word used here means just about anything.

    The Qur’an describes the next stage of the developing human embryo with the word `alaqah. This word carries various meanings including: to hang, to be suspended, to be dangled, to stick, to cling, to cleave and to adhere. It can also mean to catch, to get caught, to be affixed or subjoined. Other connotations of the word `alaqah include a leech-like substance, having the resemblance of a worm; or being of a ‘creeping’ disposition inclined to the sucking of blood. Finally, its meaning includes clay that clings to the hand and thick, clotted blood – because of its clinging together.

    I could call the embryo a sticky blob, too, and stretch and twist the words to match it in the vaguest possible way to a technical description, too…but it doesn’t make it a technical description, and it doesn’t make it informative.

    This section concludes by claiming that the “leech” interpretation of ‘alaqah is accurate, because later in development it looks, he claims, like a leech. Only to a blind man. And further, he applies this term “like a leech” to every stage in the first month of development; the accuracy of the comparison seems irrelevant.

  5. “a lump of flesh”. More of the same. Take the Arabic word (“mudghah”), throw out a bunch of definitions for the word, then force-fit them all into the actual science.

    The next stage of human development defined in the Qur’an is mudghah. This term means to chew, mastication, chewing, to be chewed, and a small piece of meat. It also describes the embryo after it passes to another stage and becomes flesh. Other meanings include something that teeth have chewed and left visible marks on; and marks that change in the process of chewing due to the repetitive act.

    No. I refuse. I’m sorry, but this is patently ridiculous. You do not get to quote the Quran talking about a chawed on scrap o’ meat, and then go on with four pages of windy exegesis claiming that corresponds to the 4th week of human development, the pharyngula stage, as if it is an insightful and detailed and specific description of an embryo. It is not. It is the incomprehending grunt of an ignorant philistine.

  6. “into bones”. Yeah. There is a mingling of fluids in sex, and at birth you have a baby with bones. Somewhere in between, bones must have formed. You do not get credit for noting the obvious without any specifics. Furthermore, turning the phrase “into bones” (‘idhaam) into this:

    There are clear parallels between the qur’anic `idhaam stage and the view modern embryology takes i.e. the development of the axial, limb and appendicular skeleton.

    is pure hyperbole and bunkum. But then, that’s all we get from Tzortzis.

  7. “clothed the bones with flesh”. Tzortzis now talks about myoblasts aggretating and migrating distally, formation of dorsal and ventral muscle masses, innervation of the tissue, and specification of muscle groups. Good god, just stop. The Quran says nothing about any of this. And then to complain that This level of detail is not, however, included in Aristotle’s description, is absurd and ironic. It’s not in Mohammed’s description, either.

    It must be noted that the migration of the myoblasts surrounding the bones cannot be seen with the naked eye. This fact creates an impression of the Divine nature of the Qur’an and reiterates its role as a signpost to the transcendent.

    Crap. The Quran doesn’t describe myoblast migration. There isn’t even a hint that Mohammed saw something you need a microscope to see.

  8. “made him into other forms”. Then Allah did all the other stuff that he needed to do to turn a chunk of chewed meat made of bone and flesh into a person. Presto, alakazam, abracadabra. Oooh, I am dazzled with the scrupulous particularity of that scientific description.

There’s absolutely nothing novel or unexplainable in the Quran’s account of development. It is a vague and poetic pair of verses about progressive development, expressed in the most general terms, so nebulous that there is very little opportunity for disproof, and they can be made to fit just about any reasonable observation. They can be entirely derived from Aristotle’s well-known statement about epigenesis, “Why not admit straight away that the semen…is such that out of it blood and flesh can be formed, instead of maintaining that semen is both blood and flesh?”, which is also a very broad statement about the gradual emergence of differentiated tissues from an amorphous fluid.

Only a blinkered fanatic could turn that mush into an overwrought, overextended, overblown, strained comparison with legitimate modern science. Tzortzis’s paper is risible crackpottery.

(Also on FtB)

William Lane Craig and the problem of pain

Kitties experience pain and suffering, which turns out to be a theological problem. If a god introduced pain and death into the world because wicked ol’ Eve was disobedient, why is god punishing innocent animals? It seems like a bit of a rotten move to afflict the obedient along with the disobedient — shouldn’t god have just stricken humanity with the wages of sin (or better yet, just womankind)?

William Lane Craig has an answer. His answer involves simply waving the problem away — animals don’t really feel pain — and he drags in science to prop up his claim. Basically, Craig is playing the creationist gambit of abusing the authority of science falsely to support his peculiar theology.

So Christian theologians of all stripes have to face the challenge posed by animal pain. Here recent studies in biology have provided surprising, new insights into this old problem. In his book Nature Red in Tooth and Claw: Theism and the Problem of Animal Suffering, Michael Murray distinguishes three levels in an ascending pain hierarchy (read from the bottom up):

Level 3: a second order awareness that one is oneself experiencing (2).

Level 2: a first order, subjective experience of pain.

Level 1: information-bearing neural states produced by noxious stimuli resulting in aversive behavior.

Spiders and insects–the sort of creatures most exhibiting the kinds of behavior mentioned by Ayala–experience (1). But there’s no reason at all to attribute (2) to such creatures. It’s plausible that they aren’t sentient beings at all with some sort of subjective, interior life. That sort of experience plausibly does not arise until one gets to the level of vertebrates in the animal kingdom. But even though animals like dogs, cats, and horses experience pain, nevertheless the evidence is that they do not experience level (3), the awareness that they are in pain. For the awareness that one is oneself in pain requires self-awareness, which is centered in the pre-frontal cortex of the brain–a section of the brain which is missing in all animals except for the humanoid primates. Thus, amazingly, even though animals may experience pain, they are not aware of being in pain. God in His mercy has apparently spared animals the awareness of pain. This is a tremendous comfort to us pet owners. For even though your dog or cat may be in pain, it really isn’t aware of it and so doesn’t suffer as you would if you were in pain.

As is usual upon reading any argument by William Lane Craig, I find myself wondering if we shouldn’t, in the name of common decency, have him locked up or in some way isolated from the sane human population. He makes bad arguments, he makes dishonest arguments, and he seems opportunistically willing to sacrifice moral reasoning on the altar of his barbarian god. Or at least, maybe we should confiscate his pets and put them in a safer home.

A few objections popped instantly into my head when I read his essay.

  • An assertion built on a false premise is likely to be false itself. Craig (or possibly his source, Murray), misrepresent the science. They claim that the prefrontal cortex “is missing in all animals except for the humanoid primates.” This is simply false! I’ve personally done histological work and surgery on the prefrontal cortex of cats, many years ago, and you can find papers describing the prefrontal cortex of opossums, and just about any common mammal you can think of. Craig has made a truly bizarre claim, like declaring that only people have noses or something.

    Primates do have a unique histologic feature of their primary cortices, an internal granule layer that is developed to varying degrees. But it’s also present in prosimians as well as all primates, so you can’t argue that it is unique to ‘humanoid primates’, and you can’t claim that it’s necessary and sufficient for self-awareness. If a bushbaby is going to be declared self-aware because it has an internal granule layer, it seems ridiculous to argue that other mammals with a similar or greater degree of cortical development are excluded from the club on the basis of this one detail.

    Scientists are supposed to talk about the evidence. Theologians are apparently not only exempt, but they get to fabricate their evidence. Also, I’m used to hearing theologians babble about the nonexistent as if it were real, but this is the first time I’ve heard one argue that a real structure is nonexistent.

  • There is a real issue here: we can identify pain neurons in insects and fish and all kinds of animals — they’re ubiquitous. But you could ask about the slippery problem of consciousness, and wonder whether there is a real difference between reflexive aversion to a noxious stimulus and a more substantial awareness of pain. There are people who argue that non-human animals are not thinking and self-aware like we are, and so their perception of pain is qualitatively different.

    Unfortunately, you can’t make a binary distinction here. If we accept that humans are all aware of pain (there have been people who don’t accept that: Nazi-types and racists have argued that Jews and blacks, for instance, are subhumans who have blunted sensitivities), it’s hard to argue that chimpanzees aren’t also aware — they exhibit all the signs of stress, of learning aversion, of memory and recall of unpleasant experiences, and their behavior is identical to ours: they make it known that they don’t like needles or fear snakes or suffer pain and distress at their discomfort and the discomfort of others. And if you admit chimps, where do you draw the line? Dogs also exhibit all of those behaviors; they even show empathy when people are injured or unhappy.

    How can anyone who has known a dog deny that they are capable of perceiving pain in fairly complex ways?

    But it really is a continuum. I haven’t been able to tell if cats feel much empathy — they don’t show it, but I have no way to see what interesting (or terrifying) cognitive wheels are spinning in a cat’s brain. I know they react to their own pain in very emotional ways, and I’ve seen mother cats respond with what looks like affection and protectiveness to their kittens…and I would not assume that a cat’s aversive reaction to getting cut is all a superficial reflex, and therefore anesthesia is unnecessary in operating on them. That is the road of the psychopath.

    Again, scientists rely on the evidence: if I see an animal struggling and making frightened noises and fighting to avoid a painful experience, and if it shows recognition of the circumstances of that pain in the future, I’m going to assume that it feels pain and is in some sense aware of its situation. Theologians are apparently able to see a cat or dog in the throes of agony and declare that it isn’t really suffering, no, not like you or me. Hey, theologians and psychopaths have something in common!

  • Let us consider the implications of Craig’s worldview. If this property of awareness sets humans apart from animals, making our suffering have a greater moral significance than that of animals, and if that awareness is a product of a specific neuroanatomical structure, the prefrontal cortex (or more specifically, a well-developed internal granule cell layer in that cortex), then what is the status of a human that lacks that all-important, very specific pattern of neuronal connectivity?

    I’m thinking, of course, of the embryo. The internal granule cell layer does not pop into existence at the moment of fertilization — it arises much later, gradually, as the brain matures. Cortical wiring is an ongoing process after birth, as well — the microstructure of the human brain changes amazingly during the first couple of years of life. If we’re going to claim that an adult dog, despite appearances, isn’t really aware of pain, shouldn’t we be saying the same thing about the embryo?

    I mean, sure, babies squall and scream and flail about at the slightest discomfort, but how do you really know that they’re actually conscious? Maybe they’re just bio-reflexive hunks of meat until the final bits of their cortical cytoarchitecture snap into place, and we should be unperturbed by their struggles. They’re not really human yet, after all — god hasn’t given them that second-order awareness that they need in order to be conscious of their deontological status as the product of original sin, you know.

    I don’t know of any scientist — or sane human being — who could make that argument seriously. Again, it’s about the evidence; they exhibit the symptoms of feeling pain, they have some complex cerebral machinery that we think is likely capable of processing experiences in complex ways (but we don’t know for sure — we don’t have a parts list of neuroanatomical correlates that are sufficient to generate consciousness), so the humane assumption is that yes, babies perceive pain. Apparently, this is a much more ambiguous issue for theologians, if they had any consistency in their views. Oh, but wait — theologians. Evidence, consistency, reason are not highly valued properties of theological arguments. If they were, it would suggest that Craig ought to rethink his dogmatic anti-abortion stance.

Sorry, Mr Craig, but pain is still a big problem for your religion, and you don’t get to shoo it away or drag in the mangled, bleeding body of a butchered science in agony to act as a scarecrow and distract people from your absence of evidence.

(Also on FtB)

How many genes does it take to make a squid eye?

This is an article about cephalopods and eye evolution, but I have to confess at the beginning that the paper it describes isn’t all that interesting. I don’t want you to have excessive expectations! I wanted to say a few words about it, though, because it addresses a basic question I get all the time, and while I was at it, I thought I’d mention a few results that set the stage for future studies.

I’m often asked to resolve some confusion: the scientific literature claims that eyes evolved multiple times, but I keep saying that eyes show evidence of common origin. Who is right? Why are you lying to me, Myers? And the answer is that we’re both right.

Eyes evolved independently multiple times: the cephalopod eye evolved about 480 million years ago, and the vertebrate eye is even older (490 to 600 million years), but both evolved long after the last common ancestor of molluscs and chordates, which lived about 750 million years ago. The LCA probably did not have an image-forming eye at all.

And that’s the key point: a true eye is a structure that has an image forming element, a retina, and some kind of morphological organization that allows a distant object to form a pattern of light on that retina. That organization can be something as simple as a cup-shaped depression or pinhole lens, or as elaborate as our camera eye, or an insect’s compound eye, or the mirror eyes of a scallop. An eye is photoreceptors + structure. Eyes have evolved multiple times; they’ve even evolved multiple times within the phylum Mollusca, and different lineages have adopted different strategies for forming images.

i-0f6286e48f36b86c30ae81bdbfc6f415-eye_phylo-thumb-500x210-70144.jpeg
(Click for larger image)
Phylogenetic view of molluscan eye diversification. Camera eyes were independently acquired in the coleoid cephalopod (squids and octopuses) and vertebrate lineages.

The LCA probably didn’t have an eye, but it did have photoreceptors, and the light sensitive cells were localized to patches on the side of the head. It even had two different classes of photoreceptors, ciliary and rhabdomeric. That’s how I can say that eyes demonstrate a pattern of common descent: animals share the same building block for an eye, these photoreceptor cells, but different lineages have assembled those building blocks into different kinds of eyes.

Photoreceptors are fundamental and relatively easy to understand; we’ve worked out the full pathways in photoreceptors that take an incoming photon of light and convert it into a change in the cell’s membrane properties, producing an electrical signal. Making an eye, though, is a whole different matter, involving many kinds of cells organized in very specific ways. The big question is how you evolve an eye from a photoreceptor patch, and that’s going to involve a whole lot of genes. How many?

This is where I turn to the paper by Yoshida and Ogura, which I’ve accused of being a bit boring. It’s an exercise in accounting, trying to identify the number and isolate genes that are associated with building a camera eye in cephalopods. The approach is to take advantage of molluscan phylogeny.

As shown in the diagram above, molluscs are diverse: it’s just the coleoid cephalopods, squid and octopus, that have evolved a camera eye, while other molluscs have mirror, pinhole, or compound eyes. So one immediate way to narrow the range of relevant genes is a homology search: what genes are found in molluscs with camera eyes that are not present in molluscs without such eyes. That narrows the field, stripping out housekeeping genes and generic genes involved in basic cellular processes, even photoreception. Unfortunately, it doesn’t narrow the field very much: they identified 5,707 candidate genes that might be evolved in camera eye evolution.

To filter it further, the authors then looked at just those genes among the 5,707 that were expressed in embryos. Eye formation is a developmental process, after all, so the interesting genes will be expressed in embryos, not adults (a sentiment with which I always concur). Unfortunately, development is a damnably complicated and interesting process, so this doesn’t narrow the field much, either: we’re down to 3,075 candidate genes.

Their final filter does have a dramatic effect, though. They looked at the ratio of non-synonymous to synonymous nucleotide changes in the candidate genes, a common technique for identifying genes that have been the target of selection, and found a grand total of 156 genes that showed a strong signal for selection. That’s 156 total genes that are different between coleoids and other molluscs, are expressed in the embryonic eye, and that show signs of adaptive evolution. That’s manageable and interesting.

They also looked for homologs between cephalopod camera eyes and vertebrate camera eyes, and found 1,571 of them; this analysis would have been more useful if it were also cross-checked against other non-camera-eye molluscs. As it is, that number just tells us some genes are shared, but they could have been genes involved in photoreceptor signalling (among others), which we already expect to be similar. I’d like to know if certain genes have been convergently adopted in both lineages to build a camera eye, and it’s not possible to tell from this preliminary examination.

And that’s where the paper more or less stops (I told you not to get your hopes up too high!) We have a small number of genes identified in cephalopods that are probably important in the evolution of their vision, but we have no idea what they do, precisely, yet. The authors have done some preliminary investigations of a few of the genes, and one important (and with hindsight, rather obvious) observation is that some of the genes are expressed not just in the retina, but in the brain and optic lobes. Building an eye involved not just constructing an image-forming sensor, but expanding central tissues involved in processing visual information.

Fernald RD (2006) Casting a genetic light on the evolution of eyes. Science 313(5795):1914-8.

Yoshida MA, Ogura A (2011) Genetic mechanisms involved in the evolution of the cephalopod camera eye revealed by transcriptomic and developmental studies.. BMC Evol Biol 11:180.

(Also on FtB)

I wish I could go

It’s a conference, in Oregon, and it’s about The Future of Evo-Devo, all wonderful things, and it’s on 10-12 February — right in the thick of the traditional Darwin Day hoopla, the days when I’m like a big egg-laying bunny at Easter. I’m already booked for Pullman, Washington, then Florida, then Las Vegas in that week.

You’ll just have to go in my place and report back. Yes, you — the one looking around quizzically and wondering “why me?” Because I said so. Book it now. Portland, 10 February, the Nines Hotel.

Coincidentally, I’m giving a talk at UNLV that is kind of about the future of evo-devo: I’m going to be both pessimistic and optimistic, and talk about the mainstreaming of evo-devo into the discourse of evolution and development, and propose that it isn’t so much a revolution in evolution as it is developmental biologists finally adopting views much more copacetic with standard model evolutionary thinking. There may be a lynching afterwards.

(Also on FtB)

The epigenetics miracle?

Jerry Coyne is mildly incensed — once again, there’s a lot of recent hype about epigenetics, and he doesn’t believe it’s at all revolutionary. Well, I’ve written about epigenetics before, I think it’s an extremely important subject central to our understanding of development, and…I agree with him completely. It’s important, we ought to spend more time discussing it in our classes, but it’s all about the process of gene expression, not about radically changing our concepts of evolution. I like to argue that what multigenerational epigenetic effects do is blur out or modulate the effects of genetic change over time, and it might mask out or highlight allelic variation, but ultimately, it’s all about the underlying genetic differences.

Coyne mentions one journalist who claims that new discoveries in epigenetics would “make Darwin swoon,” which is a bizarre standard. Darwin knew next-to-nothing about genetics — he had his own weird version of Lamarckian inheritance — and wasn’t even equipped to imagine molecular biology, so yes, just about anything in this field would dazzle him. My freshman introductory biology course would blow Charles Darwin away — he’d have to struggle to keep up with the products of American public education.

(Also on FtB)

Simple rules for folding a gut

I learned something new today, and something surprising. I’ve opened up my fair share of bellies and seen intestines doing their slow peristaltic dance in there, and I knew in an abstract way that guts were very long and had to coil to fit into the confined space of the abdominal cavity, but I’d always just assumed it was simply a random packing — that as the gut tube elongated, it slopped and slithered about and fit in whatever way it could. But no! I was reading this new paper today, and that’s not the case at all: there is a generally predictable pattern of coiling in the developing gut, and it’s species-specific.

The midgut forms as a simple linear tube of circular cross-section running down the midline of the embryo, and grows at a greater rate than the surrounding tissue, eventually becoming significantly longer than the trunk. As the size of the developing mid- and hindgut exceeds the capacity of the embryonic body cavity, a primary loop is forced ventrally into the umbilicus (in mammals) or yolk stalk (in birds). This loop first rotates anticlockwise by 90° and then by another 180° during the subsequent retraction into the body cavity. Eventually, the rostral half of the loop forms the midgut (small intestine) and the caudal half forms the upper half of the hindgut (the ascending colon).

The chirality of this gut rotation is directed by left-right asymmetries in cellular architecture that arise within the dorsal mesentery, an initially thick and short structure along the dorsal-ventral axis through which the gut tube is attached to the abdominal wall. This leads the mesentery to tilt the gut tube leftwards with a resulting anticlockwise corkscrewing of the gut as it herniates. However, the gut rotation is insufficient to pack the entire small intestine into the body cavity, and additional loops are formed as the intestine bends and twists even as it elongates. Once the gut attains its final form, which is highly stereotypical in a given species, the loops retract into the body cavity. During further growth of the juvenile, no additional loops are formed, as they are tacked down by fascia, which restrict movement and additional morphogenesis without inhibiting globally uniform growth.

That is just plain awesome. Now I want to open up a zebrafish and look at the curling of its intestines, or better yet, peer into a larva and see if there are any predictable rules of formation. Oh, jeez, I want to look inside my own belly, although that would be a kind of self-defeating experiment.

i-09a6a8c890e239d198a7ed0075c7e511-gut.jpeg
Morphology of loops in the chick gut. a, Chick gut at embryonic day 5 (E5), E8, E12 and E16 shows stereotypical looping pattern.
b, Proliferation in the E5 (left) and E12 (right) gut tubes (blue) and mesentery (red). Each blue bar represents the average number of phospho-H3-positive cells per unit surface in 40 (E5) or 50 (E12) 10-mm sections. Each red bar represents the average number of phospho-H3-positive cells per unit surface over six 10-mm sections (E5) or in specific regions demarcated by vasculature along the mesentery (E12). The inset images of the chick guts align the proliferation data with the locations of loops (all measurements were made in three or more chick samples). Ant., anterior; post., posterior. Error bars, s.d. c, The gut and mesentery before and after surgical separation at E14 show that the mesentery shrinks while the gut tube straightens out almost completely. d, The E12 chick gut under normal development with the mesentery (left) and after in ovo surgical separation of the mesentery at E4 (right). The gut and mesentery repair their attachment, leading to some regions of normal looping (green). However, a portion of the gut lacks normal loops as a result of disrupting the gut-mesentery interaction over the time these loops would otherwise have developed.

So how do species-specific coiling patterns emerge? A naive expectation might be that there are specific genes associated with the process that selectively impose bends at specific locations along the length of the intestine — that there is genetically determined spatial information along the tube that defines how it should coil. This is not the case. Instead, the reproducible pattern of coiling is an emergent property of some general parameters of the tissues.

You do need to know some very elementary anatomy to know what’s going on here. The gut begins embryonically as a simple, straight tube, fixed at both ends at the mouth and anus. Initially, the gut is the same length as the body, and is suspended from the back of the body cavity by a continuous sheet of tissue, the mesentery, that is also the same length as the gut. But then what happens is that the gut elongates, while the mesentery grows much more slowly. This difference in growth rates means that the gut is under compression along its length, restrained by the mesenteries, which causes it to periodically buckle.

One way to test the role of the mesentery is to remove it. If you carefully cut it away from the gut, as is shown in (c) and (d) of the figure above, it straightens out — in a fully relaxed state, without the compression of the mesenteries, the gut is straight and linear. You can do partial cuts, too, and wherever a stretch of gut is released from the mesentery constraint, it uncoils.

Take it another step. Is this how generic tubes and sheets interact? The authors took a rubber tube of length Lt, and a rubber sheet of length Lm, where Lm is less than Lt. They stretched the rubber sheet to length Lt, stitched it to the rubber tube, and then let it go. Voila, it spontaneously coiled into a configuration (b) that closely resembles the chicken gut (c).

i-571204bbea1fb30c242e8d1712da42c8-gut_model.jpeg
Rubber simulacrum of gut looping morphogenesis. a, To construct the rubber model of looping, a thin rubber sheet (mesentery) was stretched uniformly along its length and then stitched to a straight, unstretched rubber tube (gut) along its boundary; the differential strain mimics the differential growth of the two tissues. The system was then allowed to relax, free of any external forces. b, On relaxation, the composite rubber model deformed into a structure very similar to the chick gut (here the thickness of the sheet is 1.3 mm and its Young’s modulus is 1.3 MPa, and the radius of the tube is
4.8 mm, its thickness is 2.4 mm and its Young’s modulus is 1.1 MPa. c, Chick gut at E12. The superior mesenteric artery has been cut out (but not the mesentery), allowing the gut to be displayed aligned without altering its loop pattern.

This is qualitatively convincing — they do look very similar, and at this point I’m willing to believe that mechanical forces are sufficient to explain the coiling pattern. The authors take another step, though: they bring out the math and get all quantitative. This is a reasonable idea; from the model above, it does look like the shape is reducible to a small number of parameters, so it’s a manageable problem. So brace yourself: a little math coming right up.

We now quantify the simple physical picture for looping sketched above to derive expressions for the size of a loop, characterized by the contour length, λ, and mean radius of curvature, R, of a single period. The geometry of the growing gut is characterized by the gut’s inner and outer radii, ri and ro, which are much smaller than its increasing length, whereas that of the mesentery is described by its homogeneous thickness, h, which is much smaller than its other two dimensions. Because the gut tube and mesentery relax to nearly straight, flat states once they are surgically separated, we can model the gut as a one-dimensional elastic filament growing relative to a thin two-dimensional elastic sheet (the mesentery). As the gut length becomes longer than the perimeter of the mesentery to which it is attached, there is a differential strain, ε, that compresses the tube axially while extending the periphery of the sheet. When the growth strain is larger than a critical value, ε* the straight tube buckles, taking on a wavy shape of characteristic amplitude A and period λ>A. At the onset of buckling, the extensional strain energy of the sheet per wave- length of the pattern is Um∝Emε2hλ2, where Em is the Young’s modulus of the mesentery sheet. The bending energy of the tube per wavelength is Ut∝EtItκ2λ, where κ ∝ A/λ2 is the tube curvature, It ∝ ro4-ri4 is the moment of inertia of the tube and Et is the Young’s modulus of the tube. Using the condition that the in-plane strain in the sheet is ε* ∝ A/λ and minimizing the sum of the two energies with respect to λ then yields a scaling law for the wavelength of the loop:

i-167b774c963520e54424b9923991feef-gut_form.jpeg

Did you get all that? If not, don’t worry about it. What it all means is that we can measure general properties of gut tissues, plug the parameters into these formulas, and ask a computer to predict what the gut should look like in a numerical simulation. And it works!

i-a3c0b19e75c4d2c93a72fd781ab6a694-gut_sim.jpeg
Predictions for loop shape, size and number at three stages in chick gut development. a, Comparisons of the chick gut at E16 (top) with its simulated counterpart (bottom). b, Scaled loop contour length, λ/ro, plotted versus the equivalently scaled expression from equation (3) for the chick gut (black squares), the rubber model (green triangles) and numerical simulations (blue circles). The results are consistent with the scaling law in equation (1). c, Scaled loop radius, R/ro, plotted versus the equivalently scaled expression from equation (4) for the chick gut, the rubber model, and numerical simulations (symbols are as in b). The results are consistent with the scaling law in equation (2). Error bars, s.d.

At this point, you should be saying enough — that’s more than enough awesome to convince you that they’ve determined the rules that shape the gut. But no, they go further: all the above work is in chickens, so they reach out and start disemboweling other species, and ask if their formulas work to describe their gut coiling, too. Would you be surprised to learn that it does?

i-2a05e702aac44b304076d83089244467-gut_species.jpeg
Comparative predictions for looping parameters across species. a, Gut looping patterns in the chick, quail, finch and mouse (to scale) show qualitative similarities in the shape of the loops, although the size and number of loops vary substantially. b, Comparison of the scaled loop contour length, λ/ro, with the equivalently scaled expression from equation (3) shows that our results are consistent with the scaling law in equation (1) across species. Black symbols are for the animals shown in a, other symbols are the same as in Fig. 4b. c, Comparison of the scaled loop radius, R/ro, with the equivalently scaled expression from equation (4) shows that our results are consistent with the scaling law in equation (2) across species (symbols are as in b). In b and c, points are reported for chick at E8, E12 and E16; quail at E12 and E15; finch at E10 and E13; and mouse at E14.5 and E16.5. Error bars, s.d.

What makes this a beautiful result is that it’s a perfect illustration of the principles D’Arcy Wentworth Thompson laid out in his book, On Growth and Form (and even the title of the paper is a nod to that classic of developmental biology). Sometimes, simple mathematical rules govern the patterns we see in developing systems, whether it’s the Fibonacci spirals we see in the head of a sunflower or the coils of a nautilus shell, or tangled loops of our intestines. The form is not laid out in tightly-coded, case-by-case specification in the genome, but by the genetic definition of only a few parameters, in this case the relative rates of growth of two adherent tissues and the compression they impose on an elongating tube, from which a lovely arrangement flowers elegantly.

Savin T, Kurpios NA, Shyer AE, Florescu P, Liang H, Mahadevan L, Tabin CJ (2011) On the growth and form of the gut. Nature 476:57-63.

(Also on FtB)

The greatest science paper ever published in the history of humankind

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.

Cephalopods evolved from monoplacophoran-like ancestors in the Cambrian, about 530 million years ago. Monoplacophorans are simple, limpet-like molluscs; they crawl about on the bottom of the ocean under a cap-like shell, foraging snail-like on a muscular foot. The early cephalopods modified this body plan to rise up off the bottom and become more active: the flattened shell elongated to become a cone-like structure, housing chambers for bouyancy. Movement was no longer by creeping, but used muscular contractions through a siphon to propel the animal horizontally. Freed from its locomotor function, the foot expanded into manipulating tentacles.

i-a4650a364628b045d3f57a3baf0e7529-monoplacophoran.jpeg

These early cephalopods, which have shells common in the fossil record, would have spent their lives bobbing vertically in the water column, bouyed by their shells, and with their tentacles dangling downward to capture prey. They wouldn’t have been particularly mobile — that form of a cone hanging vertically in the water isn’t particularly well-streamlined for horizontal motion — so the next big innovation was a rotation of the body axis, swiveling the body axis 90° to turn a cone into a torpedo. There is evidence that many species did this independently.

i-f8e43ceb7154a2f6b4c1b890e7ac4f64-ceph_rotation-thumb-500x331-67138.jpeg
The tilting of the body axes of extant cephalopods. This was a result of a polyphyletic and repeated trend towards enhanced manoeuverability. The morphological body axes (anterior-posterior, dorso-ventral) are tilted perpendicularly against functional axes in the transition towards extant cephalopods.

We can still see vestiges of this rotation in cephalopod embryology. If you look at early embryos of cephalopods (at the bottom of the diagram below), you see the same pattern: they are roughly disc-shaped, with a shell gland on top and a ring of tentacle buds on the bottom. They subsequently extend and elongage along the embryonic dorsal-ventral axis, which becomes the anterior-posterior axis in the adult.

i-4ad43bc29c4b1d48673f4cd0de6356a5-ceph_comp_embryo-thumb-450x786-67111.jpeg
In extant cephalopods the body axes of the adult stages are tilted perpendicularly versus embryonic stages. As a con- sequence, the morphological anterior-posterior body axis between mouth and anus and the dorso-ventral axis, which is marked by a dorsal shell field, is tilted 908 in the vertical direction in the adult cephalopod. Median section of A: Nautilus, B: Sepia showing the relative position of major organs (Drawings by Brian Roach). C: shared embryonic features in embryos of Nautilus (Nautiloidea) and Idiosepius (Coleoidea) (simplified from Shigeno et al. 2008 [23] Fig. 8). Orientation of the morphological body axes is marked with a compass icon (a, anterior; d, dorsal; p, posterior; v, ventral; dgl, digestive gland; gon, gonad; ngl, nidamental gland).

The next division of the cephalopods occurred in the Silurian/Devonian, about 416 million years ago, and it involved those shells. Shells are great armor, and in the cephalopods were also an organ of bouyancy, but they also greatly limit mobility. At that early Devonian boundary, we see the split into the two groups of extant cephalopods. Some retained the armored shells; those are the nautiloids. Others reduced the shell, internalizing it or even getting rid of it altogether; those are the coleoids, the most successful modern group, which includes the squids, cuttlefish, and octopuses. Presumably, one of the driving forces behind the evolution of the coleoids was competition from that other group of big metazoans, the fish.

The nautiloids…well, the nautiloids weren’t so successful, evolutionarily speaking. Only one genus, Nautilus has survived to the modern day, and all the others followed the stem-group cephalopods into extinction.

The coleoids, on the other hand, have done relatively well. The number of species have fluctuated over time, but currently there are about 800 known species, which is respectable. The fish have clearly done better, with about 30,000 extant species, but that could change — there are signs that cephalopods have been thriving a little better recently in an era of global warming and acute overfishing, so we humans may have been giving mobile molluscs a bit of a tentacle up in the long evolutionary competition.

There was another major event in coleoid history. During the Permian, about 276 million years ago, there was a major radiation event, with many new species flourishing. In particular, there was another split: between the Decabrachia, the ten-armed familiar squid, and the Vampyropoda, a group that includes the eight-armed octopus, the cirroctopodes, and Vampyroteuthis infernalis. The Vampyropoda have had another locomotor shift, away from rapid jet-propelled movement to emphasizing their fins for movement, or in the case of the benthic octopus, increasing their flexibility to allow movement through complex environments like the rocky bottom.

Time for the big picture. Here’s the tree of cephalopod evolution, using dates derived from a combination of the available fossil evidence and primarily molecular clocks. The drawings illustrate the shell shape, or in the case of the coleoids, the shape of the internal shell, or gladius, if they have one.

i-205e51c0850d23812a20e3bd6bf7010f-ceph_lineage-thumb-500x631-67114.jpeg
A molecularly calibrated time-tree of cephalopod evolution. Nodes marked in blue are molecular divergence estimates (see methods in Supplemental Material). The divergence of Spirula from other decabrachiates are from Warnke et al. [43], the remaining divergences are from analyses presented in this paper. Bold lineages indicate the fossil record of extant lineages, stippled lines are tentative relationships between modern coleoids, partly based on previous studies [41, 76, 82] and fossil relationships are based on current consensus and hypoth- eses presented herein. Shells of stem group cephalopods and Spirula in lateral view with functional anterior left. Shells of coleoids in ventral view with anterior down. The Mesozoic divergence of coleoids is relatively poorly resolved compared to the rapid evolution of Cambro- Ordovician stem group cephalopods. Many stem group cephalopod orders not discussed in the text are excluded from the diagram.

The story and the multiple lines of evidence hang together beautifully to make a robust picture of cephalopod evolution. The authors do mention one exception: Nectocaris. Nectocaris is a Cambrian organism that looks a bit like a two-tentacled, finned squid, which doesn’t fit at all into this view of coleoids evolving relatively late. The authors looked at it carefully, and invest a substantial part of the review discussing this problematic species, and decided on the basis of the morphology of its gut and of the putative siphon that there is simply no way the little beast could be ancestral to any cephalopods: it’s a distantly related lophotrochozoan with some morphological convergence. It’s internal bits simply aren’t oriented in the same way as would fit the cephalopod body plan.

So that’s the state of cephalopod evolution today. I shall be looking forward to the Next Great Paper, and in particular, I want to see more about the molecular biology of tentacles — that’s where the insights about the transition from monoplacophoran to cephalopod will come from, I suspect.

Kröger B, Vinther J, Fuchs D (2011) Cephalopod origin and evolution: A congruent picture emerging from fossils, development and molecules: Extant cephalopods are younger than previously realised and were under major selection to become agile, shell-less predators. Bioessays doi: 10.1002/bies.201100001.

A little cis story

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.

i-d83d945e8def6fc2ca534e29acaec036-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.

Most of the DNA here is not transcribed. Much of it is junk — changing the sequence of those areas has no effect on the protein, and has no effect on the appearance or function of the organism. Some of it, though, is regulatory DNA, and its sequence does matter. The white boxes labeled DG2, DG3, Z, A, E, and 7 are regions called enhancers — they are not translated into protein, but their sequence affects the expression of svb/ovo. One way to think of them is that they are small parking spots for other proteins that will bind to the DNA sequences in each enhancer. These protein/DNA complexes will then fold around to make a little landing zone for the polymerase, to encourage transcription of the svb/ovo gene. This is why this is called regulatory DNA: it doesn’t actually make the svb/ovo protein itself, but it’s important in controlling when and where and how much of the svb/ovo protein will be made.

Now for some jargon; sorry, but you have to know what it is to follow along in the literature. Those little white boxes of regulatory DNA are often called cis factors, because they have to be located on the same strand of DNA as the protein-coding gene in order to work. In general, when we’re talking about cis factors, we’re talking about non-coding regulatory DNA. The complement of that is the actual coding sequence, the little gray boxes in the diagram, and those have the general name of trans factors.

There is a bit of a debate going on about the relative importance of cis and trans mutations in evolution. Proponents of the cis perspective like to point out that cis mutations can be wonderfully subtle and specific; you can make a change in an enhancer and only modify the expression of the gene in one tissue, or even a small part of one tissue, while changing a trans factor causes changes in every tissue that uses that gene product. Also, most of the cis proponents are evo-devo people, scientists who study the small variations in timing and magnitude of gene expression that lead to differences in form, so of course the kinds of changes that affect the stuff we study must be the most important.

Proponents of the trans view can point out that small changes in the coding regions of genes can also produce subtle shifts in what the genes do, and that mutations can also produce very large effects. Those cis changes appear to be little tweaks, while trans changes can run the gamut from non-existent/weak to strong, and so have great power. They also like to point out that most of the data in the literature documents trans changes between species, and that a lot of the evo-devo stuff is speculative.

It’s a somewhat silly debate, because we all know that both cis and trans effects are going to be found important in evolution, in different ways in different organisms, and that arguing about which is more important is kind of pointless — it will depend on which feature and which species you’re looking at. But the debate is also useful as a goad to urge people to look more at the subtleties and ask more questions about those enhancers, as in the paper I’m about to describe.

What is this svb/ovo gene?

i-6f9a564cbbfe589bd569f327224e5ab5-flybutt.jpeg

This is a drawing of just the back end of a fly larva, and what you should be able to see is that they’re very hairy. Dorsally, there’s a collection of small hairs called trichomes, and ventrally there are some thicker, stouter hairs called denticles. If you destroy the svb/ovo coding region, these hairs don’t form — svb is an important gene for organizing and making hairs on the cuticle of the fly. It’s name should make sense: svb is short for shavenbaby. The gene is responsible for making hairs, but when you break it with a mutation you get embryos and larvae lacking those hairs, a shaven baby.

It also has the synonym of ovo, because it has another important function in the maturation of oocytes, something I’ll skip over entirely. All you need to know is that svb/ovo is actually a large complex gene with multiple functions, and all we care about right now is its function of inducing hair development.

Now let’s look at embryos of two different species of fruit flies, Drosophila melanogaster at the top, and Drosophila sechellia at the bottom. D. melanogaster is clearly hairier than D. sechellia, and you might be wondering if svb is the gene making a difference here, and if you’re following the debate, you might be wondering whether this is a change in the trans coding region or the cis regulatory region.

i-a1c398554f3f1549dcb739ad80f4e8d3-twoflies.jpeg

One way to figure this out is to sequence and compare maps of the svb region in multiple fly species and ask where the actual molecular differences are. This isn’t trivial: D. melanogaster and D. sechellia have been diverging for half a million years, and there have been lots of little changes all over the place, many of them expected to be neutral. What was done to narrow the search was to compare the sequences of five different Drosophila species with hairy embryos to the relatively naked D. sechellia, and ask which changes were unique to the less hairy form.

A hotspot lit up in the comparison: there is one region, about 500 base pairs long, in the enhancer labeled “E” in the diagram at the top of the page, which contained 13 substitutions and one deletion unique to D. sechellia, in 7 clusters. This is very suggestive, but not definitive; these are consistent differences, but we don’t know yet whether these molecular differences cause the differences in hairiness. For that, we need an experiment.

The experiment.

This is the cool part. The investigators built constructs containing the E enhancer coupled to the svb gene and a reporter tag, and inserted those into fly embryos and asked how they affected expression; so they could effectively put the D. sechellia enhancer into D. melanogaster, and the D. melanogaster enhancer into D. sechellia, and ask if they were sufficient to drive the species-specific pattern of svb expression. The answer is yes, mostly: they weren’t perfect copies of each other, suggesting that there are other elements that contribute to the pattern, but the D. sechellia enhancer produced reduced expression in whatever fly carried it, while the D. melanogaster enhancer produced greater expression.

But wait, there’s more! The species differences were caused by differences in 7 clusters within the E enhancer. The authors built constructs in which the mutations in each of the 7 clusters was uniquely and independently inserted, so they could test each mutational change one by one. The answer here was that each of the seven mutations that led to the D. sechellia pattern had a similar effect, reducing very slightly the level of svb expression. Furthermore, they had a synergistic effect: the reduction in hairs when all 7 mutations were present was not simply the sum of the individual effects of each mutation alone.

What does it all mean?

One conclusion of this work is that here is one more clear example of a significant morphological difference between species that was generated by molecular modification of cis regulatory elements. Hooray, one more data point in the cis/trans debate!

Another interesting observation is that this is a phenotype that was built up gradually, by a set of small changes to an enhancer element. D. sechellia gradually lost its trichome hairs by the accumulation of single-nucleotide changes in regulatory DNA, each of which contributed to the phenotype — a very Darwinian pattern of change.

By modifying the regulatory elements, evolution can generate distinct, focused variations. Knocking out the entirety of the svb gene is disastrous, not only removing hairs but also seriously affecting fertility. The little tweaks provided by changes to the enhancer region mean that morphology can be fine-tuned by chance and selection, without compromising essential functions like reproduction. In the case of these two species of flies, D. sechellia can have a functional reproductive system, the full machinery to make functional hairs, but at the same time can turn off dorsal trichomes while retaining ventral denticles.

It all fits with the idea that fundamental aspects of basic morphology are going to be defined, not by the raw materials used to build them, but by the regulation of timing and quantity of those gene products — that the rules of development are defined by the regulatory activity of genes, not entirely by the coding sequences themselves.

Frankel N, Erezyilmaz DF, McGregor AP, Wang S, Payre F, Stern DL (2011) Morphological evolution caused by many subtle-effect substitutions in regulatory DNA. Nature 474(7353):598-603.

It’s always good to go straight to the source

I tell other scientists all the time that their work is being appropriated by creationists who barely understand it, and that it is getting distorted to support bogus pseudoscience. Whenever you see a creationist quote a genuine science paper, you can pretty much trust that it is going to be mangled beyond recognition.

For instance, Jonathan MacLatchie raised a peculiar collection of questions to grill me with; here’s one of them.

9) If, as is often claimed by Darwinists, the pharyngeal pouches and ridges are indeed accurately thought of as vestigial gill slits (thus demonstrating our shared ancestry with fish), then why is it that the ‘gill-slit’ region in humans does not contain even partly developing slits or gills, and has no respiratory function? In fish, these structures are, quite literally, slits that form openings to allow water in and out of the internal gills that remove oxygen from the water. In human embryos, however, the pharyngeal pouches do not appear to be ‘old structures’ which have been reworked into ‘new structures’ (they do not develop into homologous structures such as lungs). Instead, the developmental fate of these locations includes a wide variety of structures which become part of the face, bones associated with the ear, facial expression muscles, the thymus, thyroid, and parathyroid glands (e.g. Manley and Capecchi, 1998).

You might be wondering about what that paper actually says, and you should. Never trust a creationist! And here’s where I get to pull Marshall McLuhan into the frame from offscreen.

Nancy Manley of the University of Georgia wrote to me today.

As a fan of both your website and of the pharyngula stages of development, I was intrigued to see the questions posed to you by ID followers before your recent talk. And kind of surprised, and bit taken aback, when one of my postdoctoral papers was cited in one of the questions – I am the Manley of Manley et al.

Since the ID questioners used a reference to one of my papers in the question, and this is actually an issue I am personally interested in from a scientific point of view, I feel compelled to answer also. In a way, it is ironic that they used this paper to illustrate their question, since it was our analysis of the pharyngeal pouch phenotype of the Hoxa3 null mice that led to our own interest in why terrestrial animals don’t have gills, and how the thymus and parathyroids may have evolved. We hypothesized that the evolution of morphology in the pharyngeal region (i.e. loss of gills and gain of pouch-derived organs like the thymus and parathyroids) was due to changes in the expression and/or function of the Hoxa3 gene. This hypothesis was proposed in a book chapter that I co-authored (Manley, NR and CC Blackburn. Thymus and Parathyroids. In Handbook of Stem Cells, Vol. 2: Embryonic Stem Cells, R. Lanza (Ed). Academic Press, 2004 v. 1:pp 391-406). I even obtained an NSF grant (now defunct) to test this hypothesis, and recently published a paper in the Proceedings of the National Academy of Sciences about it (Chen, et al., 2010, PNAS 107(23):10555-10560). We haven’t solved the problem yet, but the data so far indicate that changes in both the expression and function of Hoxa3 may have been involved in the evolution of pharyngeal region derivatives during vertebrate evolution, including loss of gills and development of pharyngeal pouch-derived organs.

I wish I could magically pull scientists out of a hat every time some po-faced creationist stooge raises a hand at one of my talks and starts lecturing me on their memorized quotes from the scientific literature. They always get them wrong.

By the way, I’ve been playing a game with MacLatchie. Every time I look into one of his citations, I go to google and type in both the author’s name and that of Harun Yahya, the Turkish creationist. It’s amazing — every time, I get a couple of quotes from one of his books, and they’re almost exactly the same as MacLatchie’s comments.

For example,
Harun Yahya also cites Manley. Compare this with what MacLatchie wrote, above.

Those human emryonic “gill slits” are just another Darwinian myth. These pharyngeal pouches do not develop into homologous structures such as lungs or gill-like structures. The developmental fate of these pouches include a wide variety of structures that become parts of the face, ear cavities, bones of the middle ear, muscles of masticulation and facial expression, the lower jaw, certain neck parts, and the thymus, thyroid, and parathyroid glands. (Manley, N.R. and Capecchi, M.R., Developmental Biology, 195 (1):1-15, 1998)

Isn’t this just weird? Now Yahya is a notorious plagiarist who rips off everything he’s written from the Christian creationist literature, and I don’t think MacLatchie is getting it from him. On the other hand, MacLatchie is a nobody, so I don’t think Yahya stole it from him. I think there’s another creationist source book somewhere, which both are borrowing from to make their claims, and I’m itching to know what it is.

The one thing I know for sure is that neither MacLatchie nor Yahya are at all original or creative, and that both are just trained parrots echoing some other source. If anyone recognizes where these claims are coming from, let me know — I’d like to go straight to the original compendium of nonsense and prune it at the root.