Flitting through Saturday at SICB

Rather than burning out, I decided I just needed a happy fun day at the SICB meetings, so I put away the notepad and flitted about from session to session to check out a semi-random subset of the diverse talks available here. So I listened to talks on jaw articulations and feeding mechanisms in cartilaginous fishes; the direct developing frog, Eleutherodactylus coqui; Hox gene expression in the fins of Polyodon (which was really cool—that curious HoxD gene flip across the digits may be a primitive condition, rather than a derived tetrapod state); biomechanical properties of spider webs; the physics of snake slithering; and the role of university based natural history museums. It was very relaxing.

One thing I wish more people in the lay public could understand is that science is just plain fun, and that scientists do things because the natural world is so beautiful and so engrossing. Maybe these scientific meetings should be accompanied by a few lectures open to the public…

How I spent another morning at SICB

Everyone can stop now, my brain is full. Seriously, this is a painful meeting: my usual strategy at science meetings is to be picky and see just a few talks in a few sessions, to avoid burnout…but at this one, I go to one session and sit through the whole thing, and at the breaks I look at the program and moan over the concurrent sessions I have to be missing. I have to come to SICB more often, that’s for sure.

I do have one major complaint, though: PowerPoint abuse. The evolution of slides has continued apace since my graduate school days, when one slide was one photograph, developed in a darkroom ourselves, and then carefully labeled with letraset lettering, photographed again on a copy stand with slide film, and then sent off for processing (usually the day before the meeting, so there was no slack for redoing anything.) Now the slides are all huge multipaneled affairs with data packed into tiny little boxes that fade in as the speaker does a tarantella on the keyboard, and it’s getting a little irritating. Most of the talks this morning would, at some point, throw up a gigantic, intricately detailed cladogram with 50 taxa and branch points all labeled and circles and arrows and scary tiny lettering all around. Any one slide legitimately represents something that the speaker could talk about for an hour, no problem, but wham-bam-zoom, they’ll run through 20 of them in 20 minutes. If the information density is going to be this high, they ought to set it up so they can beam these monster slides to our laptops over the wireless network, so we can actually try to absorb it into our heads in some way other than being battered about the cranium with it.

I spent Friday morning at the Key Transitions in Animal Evolution symposium.

  • F. Boero: Cnidarian milestones in metazoan evolution. This talk was a bit thin on the data, but it was presented more as a conceptual overview, so I let it go. The idea was simple: it was an anti-Great Chain of Being talk, pointing out that sponges and especially cnidarians were darned important creatures that ought to be appreciated for the fact that they bear the seeds of everything we consider especially essential to the bilateria. They have bilateral symmetry, many have supporting skeletons, polyp buds have an internal mass that corresponds in many ways to mesoderm, they have body cavities, the modularity of their development has affinities to bilaterian metamery, and most interestingly, cnidarian planula larvae have specialized concentrations of nerve cells that resemble a brain. One weird twist (I love weird twists) was the idea that the cnidocyst was such an incredibly potent adaptation that the cnidaria didn’t need all the elaborate complexity of the bilateria to succeed, and that maybe an important milestone that was a precursor to our evolution was the loss of cnidocysts.

  • B. F. Lang: The evolutionary transition from protists to Metazoa: mitochondrial genome organization and phylogenomic analyses based on nuclear and mitochondrial genes. I was rather far over my head in this talk; it was hardcore phylogenetic analysis of really distant branch points in our evolutionary history—this fellow is trying to puzzle out the branch point between fungi and animals. I mainly just jotted down a few names I’ll have to look up later: the Ichthyosporia, which are fungal-like cells with amoeboid stages, the Nuclearia, which are low on the branch leading to the fungi, the Capsaspora, which similarly lie on a branch leading to the animals, and the Apusozoa, bikont flagellates that have been poorly characterized so far.

  • D.K. Jacobs: Origins of sensory and neural organization in basal metazoa. The cnidarian fan club was out in force in this session. This was a talk on the identification of cnidarian genes usually associated with nervous system and sensory organ development and function, the point being that all of the precursors to our rather more elaborate neural processing system are there in jellyfish. There were a few places where I wondered if he was going a little too far—there’s no reason to assume that finding a gene that is used in the vertebrate brain in a cnidarian means that gene has a similar function there—but still an interesting talk. One cute idea was that the choanocytes of sponges can also be thought of as sensory organs, and also that neural genes seem to share functions with nephridia/kidneys, too, raising the possibility of a primitive link between excretion and the origins of the nervous system. (Watch Fox News, and this possibility will seem even more likely).

  • G. Wagner: Do genome duplications play a role in key transitions? This is the second time I’ve heard this Wagner fellow talk, and he keeps making me think. He brought up a familiar correlation: in vertebrate evolution, we see signs that there are major gene duplications at the same time that we see major radiations. In the vertebrate lineage, for instance, we see two whole genome duplications, and the conceit is that these increases in genetic material provided the substrate for more sophisticated developmental events that were the source of our success; similarly, the even more successful teleosts show signs of a third round of duplications. Wagner objected, pointing out that there are many highly successful groups that did not exhibit these duplications (arthropods, insect, mammals, and birds, for instance), and that others, such as plants and sturgeon, have duplications but no subsequent radiation. He argued that it was an artifact, not evidence of a causal relationship. The rapid expansion of a lineage during an adaptive radiation would act to preserve and propagate any genetic quirks of the founding population. The duplications are neither necessary nor sufficient to instigate a key transition. One point that came up very briefly in the Q&A was that we developmental biologists are a bit obsessive about regulatory genes like the Hox genes and think those are indicative of importance, but that there are also duplications in, for instance, the glyocolytic enzymes that also correspond to the major transitions.

  • N.W. Blackstone: Foods-eye view of the transition from basal metazoans to bilaterians. This was another weird talk that came from a completely different perspective and made me think. It might actually be a little too weird, but it’s still provocative and interesting. Blackstone is looking at everything from the perspective of metabolic signaling—he’s clearly one of those crazy people coming out of the bacterial tradition. Cells communicate with one another with the byproducts of metabolism, where the redox state of membrane proteins are read as indicators of the internal state of the cells (he later calls this “honest signaling”, because there aren’t any intermediates between the cell and the expression of its metabolic state). The big innovation in the eukaryotes was to escape volume constraints by folding their chemiosmotic membranes into the interior of the organism, and the major animal innovation was the evolution of the mouth, which allowed specialized acquisition and processing of food patches. Subsequent evolution was to allow the animal to sense and seek out and exploit food patches in an environment where they were dispersed in a non-uniform manner. Another interesting tangent was the question of cancer: long-lived sponges and cnidarians don’t get cancer. His explanation was that it was because their cells use that “honest” metabolic signaling, so that rogue cells don’t have a way to trick the organism into allowing them to use more resources than they actually need; the only way to signal is to exhibit genuine metabolic distress, and cells with metabolic problems will die. Our cells have these indirect, multi-layered signaling mechanisms that allow cancer cells to “lie” to the organism as a whole.

  • P. Cartwright: Rocks and clocks: integrating fossils and molecules to date transitions in early animal evolution. Molecular phylogeny is a useful tool to find patterns, and recognize branch points; this information needs to be integrated with fossil date to calibrate the clock and anchor those events to specific dates. This work was a combined effort to put together a catalog of 18s and 28s trees, and use fossil evidence to constrain the timing of the events in a metazoan cladogram. I wasn’t entirely convinced that they’d overcome the obvious problems—fossils can provide a minimum but not a maximum age—but as an excuse to show lots of pictures of Cambrian and pre-Cambrian fossils, I wasn’t going to complain. In particular, they had some amazing cnidarian fossils from 500 million year old rocks in Utah that were pretty much indistinguishable from modern taxa; jellyfish definitely are in a good niche. In her final table of conclusions (which flew by much too quickly!), she pinned the origin of the metazoa to 950mya, the deuterostomes to 539mya, the lophotrochozoa to 537mya, the ecdysozoa to 541mya, and the placozoa to 61mya (!). The clustering of those significant groups to right around the Cambrian was an indication that the Cambrian explosion was real.

  • M. Q. Martindale: The developmental basis of body plan organization in the Eumetazoa. Uh, Mark can talk really, really fast. My notes are a rather unreadable scrawl as I tried to keep up. A general point: he emphasized that much of what we can expect to see from developmental biologists is going to look like the intricate ‘circuit diagrams’ that Eric Davidson has published, where the fundamental unit is a network of gene interactions that define a cell state. He showed Davidson’s endomesoderm specification kernel for echinoderms, for instance, and then went through each of the genes involved and showed that they are all also present in Nematostella, and that they are almost all involved in endomesoderm specification there, as well. While the network has not been identified in the cnidarian, only the components, I do’t think we’ll be too surprised to see similar interactions appear as the details are worked out.

  • D.J. Miller: Implications of cnidarian gene expression data for the origins of bilaterality: is the glass half full or half empty. Where Martindale was all about the similarities, Miller was all about the differences. He’s working with a cnidarian, too, but a different one, Acropora. He was also explaining the expression of important early patterning genes, but one very interesting difference is that he looked at Emx and Otx, homologs to anterior-posterior genes in the bilateria that are expressed in the anterior end of those animals—but are expressed at opposite ends of the Acropora planula from each other. While some gene functions are conserved, there is no simple correspondence along the body axis.

  • J. Extavour: Urbilaterian reproduction. A different sort of talk: this one was about the nature of Urbilaterian germ cells. She made the case that one of the key steps necessary to the evolution of true multicellularity was the sequestration of a distinct stem cell population that was specialized to minimize mutation with a greatly reduced mitotic rate, reduced transcription, and with mechanisms to reduce the activity of transposable elements. This was part of the process of making the fitness of individual cells take a backseat to the overall fitness of the organism.

  • P.W.H. Holland: More than one way to make a worm. This talk was fun. He started with the idea of the worm, a flexible, elongated, motile tube, and showed that “worm” was a successful form that one could find scattered across the phyla of the bilateria, and that the urbilaterian was almost certainly a worm. He then raised two questions: are there examples of more derived forms that have secondarily given up features to revert to “wormness” (he gave one example, arguing that the hagfish was basically a chordate worm); and more interestingly, are there any examples of organisms that have independently evolved into a worm? He then showed us a movie of a creature that definitely looked like a worm; on first sight, it looked like a nematode, but rather than undulating and crawling it did a strange corkscrew curl. It’s called Buddenbrockia, and it’s a parasite found inside bryozoans. closer examination showed that it is a sealed hollow tube, completely mouthless and without a gut, and with no sensory organs, and that its interior is lined with 4 blocks of longitudinal muscle. It looked like something from outer space, if you asked me. Inside that tube, though, can be found flagellated spores that look like myxozoans. Molecular phylogeny reveals that it is a myxozoan, and that it is nested within the cnidaria. The idea is that this wormlike animal was built by breaking down a cnidarian and building it up again, and so represents a worm that has evolved independently of the Eubilateria—a worm is apparently a kind of universally basic form to take. Very cool!

How I spent my morning at SICB

Here’s what I heard this morning. Wonderful stuff, all of it, and I’m having a grand time. This is a quick summary, and now I have to rush back to the meeting for more.

  • S. Kuratani: Craniofacial evolution from a developmental perspective. This was a lamprey and hagfish talk, comparing them to vertebrates. Hox gene expression patterns in lamprey, which assign anterior-posterior positional information, are very similar to those in vertebrates, but there is no temporal colinearity—timing is all over the place. There is no apparent dorsal-ventral patterning of Dlx gene expresion. They’ve collected a small number of hagfish eggs and embryos and gotten good histology (unlike much of the older work). The neural crest forms by delamination and migrates into the intersegmental spaces; it also looks very much like the vertebrate pattern.

  • A. Abzhanov: Pecking at the origin of avian morphological variation. This was the story recently published in Nature on the molecular basis of beak shapes in the Galapagos finches. In short, Bmp4 expression is important in regulating the width and depth of the beak, and Calmodulin expression affects the length; there is modularity in controlling the different beak dimensions. He promises to look in the future at a couple of different phenomena: a finch with a deep but narrow beak might help sort out the factors involved in those two dimensions, he’s examining Galapagos mockingbirds, and he’s looking at muscle-bone coupling, since muscles have to follow changes in bone structure.

  • J. Helms: Unraveling the basis for species specific facial form. More birds! Here the question is the role of differences in neural crest potential that affect beak/face morphology. In some cool transplant experiments, she put neural crest from a duck embryo (long, flat bill) into a quail (short, pointy beak), and found that the quail embryos from flatter, broader bills. The converse experiment, quail neural crest into a duck embryo, produced duck embryos with short, pointed beaks. Microarray analysis of the genes with differential patterns of expression in these two species revealed that the gene differences were turned on at the phylotypic stage, when the facial prominences were indistinguishable, and the gene expression patterns at the phenotypic stage were simply maintained or held over — there is a hidden variation at the phylotypic stage that precedes the morphological differentiation. She also showed some promising work for the future, looking at the molecular basis for beak variation in different breeds of pigeons.

  • Y. Yamamoto: Why cavefish lost their eyes? Natural selection or neutral theory. Hey, get the latest issue of Seed — I summarized this story already! Even shorter summary: it’s indirect selection for a pleiotropic tradeoff.

  • G. Schlosser: How old genes make a new head: recent insights into development and evolution of neural crest and placodes in vertebrates. This is a neat little story about structural innovations in the evolution of the head. In addition to brain and ectoderm in the head, you’ve got two other in-between populations of plastic and critical cells: the neural crest, migratory cells that contribute to a host of tissues, and placodes, or ectodermal thickenings, that form structures like ears, lenses, lateral lines (if you had a lateral line), etc. Both populations arise at the neural plate boundary. One evolutionary scenario is that the boundary population appeared first, and then later subsets specialized to form neural crest and placodes; this model emphasizes a common origin for both. Schlosser presented his evidence and argument that they were unique from the beginning: placods are derived from the ectodermal side of the boundary, while neural crest are from the neural side.

  • L.Z. Holland: Heads or tails? Amphioxus and the evolution of axial patterning in chordates. This was a very thorough summary of comparative patterns of early gene expression in Amphioxus and frogs, fish, and all those other excessively complicated derived forms. She made the case that in many ways Amphioxius is a basal chordate. and that it has great advantages for studying axis formation and gastrulation: cell movements are minimal and simple, and you can see gene expression domains untangled from all the smearing of the extensive cell movements we see in, for instance, a frog. Among the interesting conclusions are the idea that differential Wnt gene expression is instrumental in specifying the anterior and posterior ends of the animal, and that gradients of retinoic acid (which directly target Hox gene expression) sets up positional information along the A/P axis in between.

  • G.P. Wagner: Linking the evolution of genes with the evolution of morphological characters. This was the first of two talks that set a different tone. Wagner pointed out that the developmental approach favored so far is excellent for sorting out what genes affect what other genes and are associated with the morphological differences that arise during development, but that they don’t tell you what the molecular correlates of those differences are: what specifically are the sequence changes in the sonic hedgehog gene or its regulators that cause expansion of its domain in blind cavefish? He argued that evolutionary genetics can identify candidate molecular differences as part of a program of working out the precise details of evolutionary/developmental change. Readers of Carroll’s work and its emphasis on the importance of cis regulatory elements will be interested that Wagner goes the other way, and is much more interested in the evolution of transcription factors. He gave a couple of reasons: 1) the specificity of gene regulation arises from protein-protein interactions in regulatory complexes. While there is much emphasis on the conserved sites that bind DNA in an individual protein, that is a small part of the whole, and these proteins are often poorly conserved out in the 80% that doesn’t stick to DNA, but contacts other proteins. 2) Changes in these proteins change functionality in the organims in evolution. 3) There is evidence of directional selectivity in transcription factors. 4) It’s much easier to work with sequences that are actually expressed (ah, pragmatism!). In detail, he discussed the Hoxa13 gene in zebrafish, which has been duplicated again in teleosts into Hoxa13a and Hoxa13b forms. The Hoxa13a gene is associated with a quirky morphological feature of the cypriniform fish that we zebrafish people are familiar with, the caudal extension of the yolk sac. It’s an easily assayed feature, and Wagner showed that morpholino knockdowns of Hoxa13a cleanly suppressed yolk sac extension.

  • Lark G: Links between the genetic architecture and functional morphology of the canid skeleton. This talk was a radical break from the previous ones, and was almost purely genetics. I confess, I was starving and worn out and had to make a break for lunch, so I didn’t give this talk the attention it deserved or needed, but I’ll be looking into it later. Lark is looking at quantitative trait loci in Portuguese Water Dogs and the Red Fox, and arguing that there are conserved patterns of variability that have survived 10 million years of diverging evolution.

Oh, yeah, I think we’re doing a panel discussion about science media sometime today. I have heard that it’s at 4:00, but I think that’s wrong: the short outline of events lists a Media Workshop (I think that’s us!) from 7 to 9pm in the Curtis Room at the Hyatt. I’ll start panicking right after the science sessions end this afternoon and run around and find out what’s what, when, and where. They can’t start without me, can they? GrrlScientist wouldn’t abandon me, but I don’t know about that sneaky Lynch fellow.

Superclades of the Cambrian

Allow me to introduce you to a whole gigantic superclade with which many of you may not be familiar, and some other groups in the grand hierarchy of animal evolution that I’ve mentioned quite a few times before, but would like to clear the fog with some simple definitions. Consider this a brief primer in some major animal groupings. Here’s a greatly simplified cladogram; I’ve left off quite a few groups to make the story simple.

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Doushantuo embryos dethroned?

Almost ten years ago, there was a spectacular fossil discovery in China: microfossils, tiny organisms preserved by phosphatization, that revealed amazing levels of fine detail. These specimens were identified as early animal embryos on the basis of a number of properties.

  • The cells were dimpled and shaped by adjoining cells, suggesting a flexible membrane—not a cell wall. This rules out algae, fungi, and plants.
  • The number of cells within each specimen was usually a power of 2. This is something we typically see in cleaving embryos, the sequence from 1 to 2 to 4 to 8 to 16 cells.
  • They were big. Typical somatic cells in animals are 5-10 µm in diameter, but ova can be a millimeter or more in diameter, and individual blastomeres (the cells in the cleavage stage embryo) can be several hundred µm across. These cells and the whole assemblage were in that size range.
  • The individual cells were uniform in size, as seen in many cleavage stage embryos, and contained organelles arranged in a consistent pattern.
  • They were often found encapsulated in a thin membrane, similar to the protective membrane around embryos.

There are some concerns about the interpretation, though. One troubling aspect of their distribution is that they are all only in the cleavage stage: we don’t see any gastrulas, the stage at which embryonic cells undergo shape changes and begin to move in a specific, directed manner. Studies of taphonomy (analyses of the processes that lead to fossilization) have shown that these later stages are particularly difficult to preserve, which potentially explains why we’re seeing a biased sample. Another unusual bias in the sample is that all of the embryos exhibit that regularity of division that produces equal-sized blastomeres—yet many invertebrate embryos have early asymmetric cleavages that produce recognizable, stereotyped distributions of cells. That asymmetry could be a feature that evolved late, but at the same time, some of the fossils were described as resembling molluscan trefoil embryos. Why aren’t the examples of early asymmetry translated into a later asymmetry?

Now there’s another reason to question the identity of the Doushantuo microfossils: they may be bacterial.

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Genetics of virgin birth in the Komodo dragon

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I’ve just read the article on the parthenogenetic Komodo dragons in Nature, and it’s very cool. They’ve analyzed the genetics of the eggs that have failed to develop (the remainder are expected to hatch in January) and determined that they were definitely produced without the aid of a male.

We analysed the parentage of the eggs and offspring by genetic fingerprinting. In the clutches of both females, we found that all offspring produced in the absence of males were parthenogens: the overall combined clutch genotype reconstructed that of their mother exactly. Although all offspring were homozygous at all loci, they were not identical clones. Parthenogenesis was therefore confirmed by exclusion (clutches had different alleles from potential fathers) and by the fact that the probability of obtaining a clutch of homozygous individuals after sexual reproduction was very low (P<<0.0001). Sungai’s resumption of sexual reproduction confirmed that parthenogenesis was not a fixed reproductive trait (that is, it is facultative) and that asexual reproduction is likely to occur only when necessary.

That line about “all offspring were homozygous at all loci, they were not identical clones” might need a little more explanation. Mama Dragon is heterozygous at some loci, but the meiotic mechanism that produces a diploid egg means that one cleavage (most likely the second meiotic cleavage) was suppressed, so both homologous chromosomes in the resultant ovum were derived from the same replicated DNA strand. They are not clones of the mother, because they are all homozygous while she was heterozygous; they are not identical, because which of each of the paired homologous chromosomes was passed on to an individual is random.

(I’m a little confused by the statement that they offspring are homozygous at all loci, though; that would imply that there was no crossing over at all in meiosis I, which doesn’t sound right. There ought to be reduced heterozygosity but not complete homozygosity, unless reptiles are weirder than I thought.)

The other useful snippet of information is that sex determination in these reptiles is of the WW/WZ type, where the females are the heterogametic sex. Since all of the progeny of parthenogenesis are homozygous, they are all of the homogametic genotype, and therefore male.

Parthenogenesis can also bias the sex ratio: in Varanus species, females have dissimilar chromosomes (Z and W), whereas the combination ZZ produces males10, so the parthenogenetic mechanism can produce only homozygous (ZZ or WW) individuals and therefore no females.

This has theological implications, obviously. We can now understand how a female could give rise to a male by parthenogenesis: Mary Mother of God must have been a heterogametic reptoid. David Icke will be so pleased.


Watts PC, Buley KR, Sanderson S, Boardman W, Ciofi C, Gibson R (2006) Parthenogenesis in Komodo dragons. Nature 444:1021-1022.

Spongeworthy genes

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What are the key ingredients for making a multicellular animal, or metazoan? A couple of the fundamental elements are:

  • A mechanism to allow informative interactions between cells. You don’t want all the cells to be the same, you want them to communicate with one another and set up different fates. This is a process called cell signaling and the underlying process of turning a signal into a different pattern of gene or metabolic activity is called signal transduction.

  • Patterns of differing cell adhesion. But of course! The cells of your multicellular animal better stick together, or the whole creature will fall apart. This can also be an important component of morphogenesis: switching on a particular adhesion molecule (by way of cell signaling, naturally) can cause one subset of cells to stick to one another more strongly than to their neighbors, and mechanical forces will then sort them out into different tissues.

These are extremely basic functions, sort of a minimal set of cellular activities that we need to have in place in order to even begin to consider evolving a metazoan. Fortunately for our evolutionary history, these are also useful functions for a single celled organism, and while the metazoa may have elaborated upon them to a high degree, there’s nothing novel about the general processes in our make-up. The principles of signaling and transduction were first worked out in bacteria, and anyone who has a passing acquaintance with immunology will know about the adhesive properties of bacteria, and their propensity for modulating that adhesion to build complexes called biofilms.

So let’s take a look at the distribution of signaling and adhesion molecules in single-celled organisms, multicellular animals, and most interestingly, a group that is close to the division between the two (although more on the side of multicellularity), the sponges.

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We need a thousand Sagans

I’m joining in on the Carl Sagan Memorial blog-a-thon, but I can’t offer unstinting praise. Sagan wrote about biology now and then, and every time he irritated me; I always felt like arguing with him about some detail that bugged me, and I think that was actually among his virtues—he was a scientist you cared enough about to want to criticize, and he also addressed questions wide and deep enough that we all felt like this curious astronomer was touching on our part of the universe.

Here’s one example, a short excerpt from my favorite Sagan book, The Demon-Haunted World: Science as a Candle in the Dark(amzn/b&n/abe/pwll).

The blueprints, detailed instructions, and job orders for building you from scratch would fill about 1,000 encyclopedia volumes if written out in English. Yet every cell in your body has a set of these encyclopedias. A quasar is so far away that the light we see from it began its intergalactic voyage before the Earth was formed. Every person on Earth is descended from the same not-quite-human ancestors in East Africa a few million years ago, making us all cousins.

Whenever I think about any of these discoveries, I feel a tingle of exhilaration. My heart races. I can’t help it. Science is an astonishment and a delight. Every time a spacecraft flies by a new world, I find myself amazed. Planetary scientists ask themselves: “Oh, is that the way it is? Why didn’t we think of that?” But nature is always more subtle, more intricate, more elegant than what we are able to imagine. Given our manifest limitations, what is surprising is that we have been able to penetrate so far into the secrets of Nature.

At the same time that I want to tear apart his annoying analogy of the genome to a set of encyclopedias, while I deplore the incessant focus on human evolution rather than, say, the beauty of a sponge or a beetle, there’s one thing he did well: he represented the joy we can find in the natural world. That’s something we don’t communicate enough, I think, that science is this wonderful, powerful, far-reaching enterprise that reaches farther into the glories of the universe than any other idea that has ever occurred to humanity. That’s something he made explicit in the title of his book, too — the way we will beat back the darkness is to illuminate it with science.

Evolution of vascular systems

Once upon a time, in Paris in 1830, Etienne Geoffroy St. Hilaire debated Georges Léopole Chrétien Frédéric Dagobert,
Baron Cuvier on the subject of the unity of organismal form. Geoffroy favored the idea of a deep homology, that all animals shared a common archetype: invertebrates with their ventral nerve cord and dorsal hearts were inverted vertebrates, which have a dorsal nerve cord and ventral hearts, and that both were built around or within an idealized vertebra. While a thought-provoking idea, Geoffroy lacked the substantial evidence to make a persuasive case—he had to rely on fairly superficial similarities to argue for something that, to those familiar with the details, appeared contrary to reason and was therefore unconvincing. Evolutionary biology has changed that — the identification of relationships and the theory of common descent has made it unreasonable to argue against origins in a common ancestor — but that difficult problem of homology remains. How does one argue that particular structures in organisms divided by 600 million years of change are, in some way, based on the same ancient organ?

One way is sheer brute force. Characterize every single element of the structures, right down to the molecules of which they are made, and make a quantitative argument that the weight of the evidence makes the conclusion that they are not related highly improbable. I’ll summarize here a recent paper that strongly supports the idea of homology of the vertebrate and arthropod heart and vascular systems.

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