wednesday morning at Lindau, part 2

This morning was a long session broken into two big chunks, and I’m afraid it was too much for me — my recent weird sleep patterns are catching up with me, which didn’t help at all in staying alert.

Robert Huber: Intracellular protein degradation and its control

This talk was a disaster. Not because it wasn’t good, because it was; lots of fine, detailed science on the regulation of proteases by various mechanisms, with a discussion of the structure and function of proteasomes, accompanied by beautiful mandalas of protein structure. No, the problem was that this listener’s jet lag has been causing some wild precession of my internal clocks, and a quarter of the way through this talk all systems were shutting down while announcing that it was the middle of the night, and I really couldn’t cope. I’m going to have to look up some of his papers when I get home, though.

Walter Kohn: An Earth Powered Predominantly by Solar and Wind Energy

Kohn has made a documentary to illustrate the power of solar energy. It was very basic, a bit silly — John Cleese narrates it — but might be useful in educating the pubic. He showed excerpts from it, and while it was nice, it didn’t fire me up.

Peter Agre: Canoeing in the Arctic, a Scientist´s Perspective

This was a bit strange. We’ve had all these science talks on global warming, so Agre decided to just show us what we stand to lose, and showed us photos of his vacations on canoeing trips in Canada and Alaska. They were gorgeous photos, but please don’t show me your photo album when I’m crashing hard.

I think my new and revised plan is to take a nap this afternoon and try to recharge a bit. I really must be alert for tomorrow’s session with Shimomura, Chalfie, and Tsien, which are the talks I was most anticipating. There’s also a curious talk by Werner Arber on something called Molecular Darwinism which has my skeptical genes tingling; I’ve got to see what kinds of evidence he provides for that. So brain must not melt down now.

Life Ascending

I admit, I was initially put off by the mere title of Nick Lane’s new book, Life Ascending: The Ten Great Inventions of Evolution(amzn/b&n/abe/pwll). I’m one of those many biologists who is adamant about the absence of direction in evolutionary history, and ascending just sounds too much like life climbing the rungs of the ladder of life, so I picked it up in a somewhat prejudicial mood.

Have no fear, though, I was won over. Right at the beginning, he admits that it is a subjective list; his criteria for including the ten chosen evolutionary innovations are that it had to revolutionize the living world, that it was important to a significant subset of life today, that it was a product of biological (not cultural) evolution, and that it had to be iconic — it had to symbolic and arrestingly interesting to human beings. That’s fair enough; one could write a book on just the evolved properties of prokaryotes, but yeah, operons and chemical sensing and secretion and motility are of vast importance, but they’re only going to be iconic to a rather restricted set of readers. And since my own personal interests run more to metazoan innovations, I’m not going to complain about a book that gives my hobby horses a more substantial run.

Even better, though, what enlivens the book is the biochemist’s perspective: Lane isn’t so much interested in the superficial matters of morphology, but in the emergence of new properties in the molecular machinery of the cell, and how it affects the world around us. Somehow, it always thrills me when we drill down right to the interactions of molecules to explain how biology works.

So here are the ten evolutionary inventions Lane describes.

  1. Origins of life: Where and how did life arise? A review of some of the models for abiogenesis.

  2. DNA: What conditions would allow for the synthesis of nucleotides? Where did the genetic code come from?

  3. Photosynthesis: The photosynthetic pathway is a combination of two very different functional pathways — what does this tell us about their evolution?

  4. Complex cells: How did cells become more complex? A chapter on horizontal transfer and endosymbiosis — borrowing and stealing and kidnaping by ancient cells.

  5. Sex: Why do we have sexual reproduction? A question that focuses on the cytological and genetic machinery.

  6. Movement: How do organisms get around? Cytoskeletons and motor proteins, and where they came from.

  7. Sight: How did vision evolve? A fairly wide-ranging discussion of opsins and crystallins and Hox genes and the weird glow of black smokers.

  8. Hot blood: Another chapter with a little taste of everything: respiration, metabolism, insulation, and how a key feature of our physiology affects everything.

  9. Consciousness: Where did our awareness come from? You won’t be surprised to learn that Lane is a materialist — the answer lies in the wiring of the brain.

  10. Death: Why do all organisms die, and why do we even have genes that contribute to senescence and death?

So the topics aren’t that biased: only three exclusive to multicellular animals, and six that are about eukaryotes almost exclusively — and even in those our prokaryotic heritage is discussed. And really, when you’re talking about genes and biochemistry, you can’t get away from the fact that you are dealing with genuinely universal processes.

The book is also a fun read, deep enough to give you some substance, yet clearly written with the general public in mind. If you aren’t a biologist or biochemist, don’t shy away — you will be able to read this book, and you will learn a lot from it. When I was reading it, I was thinking this would be a really enjoyable text to build a freshman seminar course around. The chapters are readable and each one addresses an interesting topic in biology, bringing up both current research and pending questions, and it’s meaty enough to spark some good discussions.

A little study in contrasts

Ray Comfort has made a post on the swine flu. You know already what kind of idiotic tripe he’s going to trot out.

The spread of the so-called ‘swine flu’ demonstrates yet again how useless and sometimes deadly a mutation can be. Furthermore, as the infection spreads around the world, the search for an antidote is desperately sought, but the very fact that the virus is seen as something to be opposed actually supports the Biblical view of this world. It is always good and right to oppose sickness, but in evolutionary terms, why don’t humans simply resign themselves to it and allow the strong to survive? The evolutionary point of view would say the virus has a ‘right’ to live, so ‘good luck’ to it!

How wrong can he be? It’s hard to imagine screwing it up more. In the evolutionary point of view, we are the children of ancestors who fought off disease and lived to procreate; those who surrender to a viruses imaginary right to live, if such imaginary beings ever existed, didn’t make much of a contribution to the current gene pool.

Well, you might wonder, what will the Ray Comforts of the world do to fight the virus?

The great hope for this fallen, diseased, weatherworn world, is the return of Christ, who has promised to bring restoration, everlasting health and peace to all people.

If waiting for Jesus is his only answer, he can join his fantasy evilutionists in the graveyard. But he’s lying here, because we know what will happen if Comfort feels the stirrings of the flu — he’ll scurry to his nearest doctor to take advantage of the work of scientists who don’t think the only hope is to cry out to Jebus.

Here’s the contrast: Nick Anthis describes the molecular mechanism of the flu’s resistance to some of the drugs in our arsenal. Unsurprisingly, he doesn’t cite the Bible even once, nor does he beg for mercy from a merciful deity. He does cite the scientific literature, though, and explains the natural, material processes — those mutations — that have contributed to the potency of this strain.

Who contributes more to the health and happiness of the people of this world, scientists or bible-thumpin’ idjits?

Snails have nodal!

i-e88a953e59c2ce6c5e2ac4568c7f0c36-rb.png

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

i-9814996ee90947e59439af12f03a03db-nodal_guts.jpg

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

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

i-21bda85fe662c24fe34efc609dcbf4ac-nodal_cilia.jpg

What about snails? Snails are cool because their asymmetries are just hanging out there visibly, easy to see without taking a scalpel to their torsos (there are also internal asymmetries that we’d need to do a dissection to see, but the external markers are easier). The assymetries also appear very early in the embryo, in a process called spiral cleavage, and in the adult, they are obvious in the handedness of shell coiling. We can see shells with either a left-handed or right-handed spiral.

i-d03d89cba8e1ae44e04152b3d93bf105-nodal_spiral.jpeg
(Click for larger image)
Chirality in snails. a, Species with different chirality: sinistral
Busycon pulleyi (left) and dextral Fusinus salisbury (right). b, Sinistral (left)
and dextral (right) shells of Amphidromus perversus, a species with chiral
dimorphism. c, Early cleavage in dextral and sinistral species (based on ref.
27). In sinistral species, the third cleavage is in a counterclockwise direction,
but is clockwise in dextral species. In the next divisions the four quadrants
(A, B, C and D) are oriented as indicated. Cells coloured in yellow have an
endodermal fate and those in red have an endomesodermal fate in P. vulgata
(dextral)15 and B. glabrata (sinistral)28. L and R indicate left and right sides,
respectively. d, B. glabrata possesses a sinistral shell and sinistral cleavage
and internal organ organization. e, L. gigantea displays a dextral cleavage
pattern and internal organ organization, and a relatively flat shell
characteristic of limpets. Scale bars: a, 2.0 cm; b, 1.0 cm; d, 0.5 cm; e, 1.0 cm.

Until now, the only organisms thought to use nodal in setting up left/right asymmetries were us deuterostomes — chordates and echinoderms. In the other big (all right, bigger) branch of the animals, the protostomes, nodal seemed to be lacking. Little jellies, the cnidaria, didn’t have it, and one could argue that with radial symmetry it isn’t useful. The ecdysozoans, animals like insects and crustaceans and nematodes, which do show asymmetries, don’t use nodal for that function. This suggests that maybe nodal was a deuterostome innovation, something that was not used in setting up left and right in the last common ancestor of us animals.

That’s why this is interesting news. If a major protostome group, the lophotrochozoa (which includes the snails) use nodal to set up left and right, that implies that the ecdysozoans are the odd group — they secondarily lost nodal function. That would suggest then that our last common ancestor, a distant pre-Cambrian worm, used this molecule in the same way.

Look in the very early mollusc embryo, and there’s nodal (in red, below) switched on in one or a few cells on one side of the embryo, the right. It’s asymmetrical gene expression!

i-6daa81c2edebfc143fde371c4849c1cf-nodal_early_exp.jpeg
(Click for larger image)
Early expression of nodal and Pitx in snails. a, 32-cell stage L.
gigantea expressing nodal in a single cell. b, Group of cells expressing Pitx in
L. gigantea. c, Onset of nodal expression in B. glabrata. d, A group of cells
expressing Pitx in B. glabrata. e, 32-cell L. gigantea expressing nodal (red) in
a single cell (2c) and brachyury (black) in two cells (3D and 3c).
f-h, brachyury (black) is expressed in a symmetrical manner in progeny of 3c
and 3d blastomeres (blue triangles in g), thus marking the bilateral axis, and
nodal (red) is expressed on the right side of L. gigantea in the progeny of 2c
and 1c blastomeres, as seen from the lateral (f) and posterior (g, h) views of
the same embryo. i, A group of cells expressing nodal (red) in the C quadrant
and Pitx (black) in the D quadrant of the 120-cell-stage embryo of L.
gigantea. j, nodal (red) and Pitx (black) expression in adjacent areas of the
right lateral ectoderm in L. gigantea. L and R indicate the left and right sides
of the embryo, respectively. The black triangle in b and i, the green, yellow
and pink arrows in f and i, and the black and pink arrows in f and h point to
the equivalent cells. Scale bars: 50µm.

Seeing it expressed is tantalizing, but the next question is whether it actually does anything in these embryos. The test is to interfere with the nodal-Pitx2 pathway and see if the asymmetry goes away…and it does, in a dramatic way. There is a chemical inhibitor called SB-431542 that disrupts this pathway, and exposing embryos to it does interesting things to the formation of the shell. In the photos below, the animal on the left is a control, and what you’re seeing is a coiled shell (opening to the right). The other two views are of an animal treated with SB-431542…and look! Its shell doesn’t have either a left- or right-handed twist, and instead extends as a straight tube.

i-055b648d0eaf32f767e5cc31f9f9a19b-nodal_shell.jpeg
(Click for larger image)
Wild-type coiled and drug-treated non-coiled shells of B.
glabrata. Control animals
(e) display the normal sinistral shell morphology. Drug-treated animals
(f, g, exposed to SB-431542 from the 2-cell stage onwards) have straight
shells. f and g show an
individual, ethanol-fixed, and shown from the side (f) and slightly rotated
(g).

What this all means is that we’ve got a slightly better picture of what genes were present in the ancestral bilaterian animal. It probably had both nodal and Pitx2, and used them to build up handedness specializations. Grande and Patel spell this out:

Although Pitx orthologues have also been identified in non-deuterostomes such as Drosophila melanogaster and
Caenorhabditis elegans, in these species Pitx has not been reported in
asymmetrical expression patterns. Our results suggest that asymmetrical expression of Pitx might be an ancestral feature of the bilaterians.
Furthermore, our data suggest that nodal was present in the common
ancestor of all bilaterians and that it too may have been expressed
asymmetrically. Various lines of evidence indicate that the last common ancestor of all snails had a dextral body. If this is true, then our
data would suggest that this animal expressed both nodal and Pitx on
the right side. Combined with the fact that nodal and Pitx are also
expressed on the right side in sea urchins, this raises the possibility
that the bilaterian ancestor had left-right asymmetry controlled by
nodal and Pitx expressed on the right side of the body. Although
independent co-option is always a possibility, the hypotheses we present can be tested by examining nodal and Pitx expression and function in a variety of additional invertebrates.

It’s also, of course, more evidence for the unity of life. We are related to molluscs, and share key genes between us.

Grande C, Patel NH (2009) Nodal signalling is involved in left-right asymmetry in snails. Nature 457(7232):1007-11.

Cephalopod venoms

i-e88a953e59c2ce6c5e2ac4568c7f0c36-rb.png

The history of venoms is a wonderful example of an evolutionary process. We’re all familiar with the idea of venomous snakes, but the cool thing is that when we examine exactly what it is they’re injecting into their prey, it’s a collection of proteins that show a nested hierarchy of descent. Ancient reptiles had a small and nasty set of poisons they would use, and to improve their efficacy, more and more have been added to the cocktail; so some lizards produce venomous proteins, while the really dangerous members of the Serpentes produce those same proteins, plus a large array of others.

i-6cf230da0ba5a3497fce1fd797019ad6-lizard_venoms.jpg

So something like CRISP (Cystein RIch Secretory Protein) is common to all, but only the most refined predators add PLA2 (Phosopholipase A2) to the mix.

Now lethally poisonous snakes are nice and cute and all, but we all know where the interesting action really is: cephalopods. Let’s leave the vertebrates altogether and look at a venomous protostome clade to see what they do.

i-ff97caf7d7970f57aa4b6dc82eace617-ceph_venom_glands.gif
Relative glandular arrangements of a cuttlefish and b octopus. Posterior gland is shown in green; anterior, in blue. Orange structure is the beak.

Brian Fry, who did all that excellent work characterizing and cataloging the
pharmacy of venoms secreted by poisonous snakes, has also turned his hand to the cephalopods. He examined the products of the venom glands of octopus, squid, and cuttlefish, and found a range of proteins, some unique, and others familiar: CAP (a CRISP protein), chitinase, peptidase S1, PLA2 and others. There are a couple of interesting lessons in that list.

First, evolution doesn’t just invent something brand new on the spot to fill a function — what we find instead is that existing proteins are repurposed to do a job. This is how evolution generally operates, taking what already exists and tinkering and reshaping it to better fulfill a useful function. Phospholipase A2, for instance, is a perfectly harmless and extremely useful non-venomous protein in many organisms — we non-toxic humans also make it. We use it as a regulatory signal to control the inflammation response to infection and injury — in moderation, it’s a good thing. What venomous animals can do, though, is inject us with an overdose of this regulator to send our local repair and recovery systems berserk, producing swelling that can incapacitate a tissue. Similarly, a peptidase is a useful enzyme for breaking down proteins in the digestive system…but a poisonous snake or cephalopod biting your hand can squirt it into the tissues, and now it’s being used to digest your muscles and connective tissue. Some effective venoms are simply common proteins used inappropriately (from the perspective of the target).

Another interesting observation is that cephalopods and vertebrates have independently converged in using some of the same venoms. In part, this is a consequence of historical availability — all animals have phospholipases,, since they are important general signalling molecules, so it’s part of the collection of widgets in the metazoan toolbox from which evolution can draw. It’s also part of an inflammation pathway that can be exploited by predators, in the same way that we have shared proteins used in the operation of the nervous system that can be targeted by neurotoxins. So there is independent convergence on a specific use of these proteins as toxins, but one of the things that facilitates the convergence is a shared ancestry.

In fact, some very diverse groups seem to consistently settle on the same likely suspects in their venoms.

i-427acefb14a1c22ea42a523485acea91-venom_table.gif

But finally, there must also be physical and chemical proteins of these particular proteins that must also predispose them to use as toxins. After all, animals aren’t coopting just any protein for venoms — they aren’t injecting large quantities of tubulin or heat shock proteins into their prey. There must be something about each of the standard suspects in venoms that make them particularly dangerous. What the comparative evolutionary approach allows us to do is identify the common molecular properties that make for a good venom. As Fry explains it,

Typically the proteins chosen are from
widely dispersed multigene secretory protein families with
extensive cysteine cross-linking. These proteins are collectively much more numerous than globular enzymes,
transmembrane proteins, or intracellular protein. Although
the relative abundance of these protein types in animal
venoms may reflect stochastic recruitment processes, there
has not been a single reported case of a signal peptide
added onto a transmembrane or intracellular protein or a
hybrid protein expressed in a venom gland. A strong bias is
also evident for all of the protein-scaffold types, whether
from peptides or enzymes. Although the protein scaffolds
present in venoms represent functionally and structurally
versatile kinds, they share an underlying biochemistry that
would produce toxic effects when delivered as an “overdose”. Toxic effects include taking
advantage of a universally present substrate to cause
physical damage or causing changes in physiological
chemistry though agonistic or antagonistic targeting. This allows the new venom gland protein to have an
immediate effect based on overexpression of the original
bioactivity. Furthermore, the features of widely dispersed
body proteins, particularly the presence of a molecular
scaffold amenable to functional diversification, are features
that make a protein suitable for accelerated gene duplication and diversification in the venom gland.

To simplify, killing something with a secreted poison typically involves reusing an extant protein, but not just any protein — only a subset of the proteins in an animal’s proteome has just the right properties to make for a good venom. Therefore, we see the same small set of proteins get independently coopted into the venom glands of various creatures.

Fry BG, Roelants K, Norman JA (2009) Tentacles of venom: toxic protein convergence in the Kingdom Animalia. J Mol Evol Mar 18. [Epub ahead of print].

Neandertal genome? Or a premature announcement?

In a potentially exciting development, researchers have announced the completion of a rough draft of the Neandertal genome in a talk at the AAAS, and in a press conference, and the latest issue of Science has a number of news articles on the subject. And that is a reason for having some reservations. There is no paper yet, and science by press release raises my hackles, and has done so ever since the cold fusion debacle. Not that I think this is a hoax or error by any means, but it’s not a good way to present a scientific observation.

Also, the work has some major limitations right now. They’ve got about 60% of the genome so far, and it’s all entirely from one specimen. From the age of these bones, degradation is inevitable, so there are almost certainly corrupted sequences in there — more coverage would give me much more confidence.

With those caveats, though, there are some tantalizing hints, and the subject is so exciting that it’s understandable why there’d be rush to announce. So far, they’ve identified approximately 1000-2000 amino acid differences in the coding part of the genome (human-chimp differences are about 50,000 amino acids), but there’s no report of any detectable regulatory differences.

I’m withholding judgement until I see a real paper; for now, you have to settle for a podcast with a science journalist, which just isn’t meaty enough yet.

Basics: Sonic Hedgehog

Every time I mention this developmentally significant molecule, Sonic hedgehog, I get a volley of questions about whether it is really called that, what it does, and why it keeps cropping up in articles about everything from snake fangs to mouse penises to whale fins to worm brains. The time seems appropriate to give a brief introduction to the hedgehog family of signaling molecules.

First, a brief overview of what Sonic hedgehog, or shh, is, which will also give you an idea about why it keeps coming up in these development papers. We often compare the genome to a toolbox — a collection of tools that play various roles in the construction of an organism. If I had to say what tool Sonic hedgehog is most like (keeping in mind that metaphors should not be overstretched), it would be like a tape measure. It’s going to have multiple uses: as a straightedge, as a paperweight to hold down your blueprints, as something to fence with your coworkers on a break, and even to measure distances. It will be pulled out at multiple times during a construction job, and it’s generically useful — you don’t need one tape measure to measure windows, another to measure doors, and yet another to measure countertops. Sonic hedgehog is just like that, getting whipped out multiple times for multiple uses during development, often being used where structures need to be patterned.

Let’s dig into some of the details. I’m using the 2006 review by Ingham and Placzek for most of this summary, so if you really want to get deeper into the literature, I recommend that paper as a starting point.

[Read more…]

Evolving snake fangs

Blogging on Peer-Reviewed Research
i-3c3ae12d88b9d206fc84149b28a6cf52-fang_embryo.jpg
Ontogenetic allometry in the fang in the front-fanged Causus rhombeatus (Viperidae) displaces the fang along the upper jaw. Scale bars, 1 mm. We note the change in relative size of the upper jaw subregions: i, anterior; ii, fang; iii, posterior. d.a.o., days after oviposition.

I keep saying this to everyone: if you want to understand the origin of novel morphological features in multicellular organisms, you have to look at their development. “Everything is the way it is because of how it got that way,” as D’Arcy Thompson said, so comprehending the ontogeny of form is absolutely critical to understanding what processes were sculpted by evolution. Now here’s a lovely piece of work that uses snake embryology to come to some interesting conclusions about how venomous fangs evolved.

Basal snakes, animals like boas, lack venom and specialized fangs altogether; they have relatively simple rows of small sharp teeth. Elapid snakes, like cobras and mambas and coral snakes, are at the other extreme, with prominent fangs at the front of their jaws that act like injection needles to deliver poisons. Then there are the Viperidae, rattlesnakes and pit vipers and copperheads, that also have front fangs, but phylogenetically belong to a distinct lineage from the elapids. And finally there are other snakes like the grass snake that have enlarged fangs at the back of their jaws. It’s a bit confusing: did all of these lineages independently evolve fangs and venom glands, or are there common underpinnings to all of these arrangements?

[Read more…]

Evolving proteins in snakes

Blogging on Peer-Reviewed Research

We’ve heard the arguments about the relative importance of mutations in cis regulatory regions vs. coding sequences in evolution before — it’s the idea that major transitions in evolution were accomplished more by changes in the timing and pattern of gene expression than by significant changes in the genes themselves. We developmental biologists tend to side with the cis-sies, because timing and pattern are what we’re most interested in. But I have to admit that there are plenty of accounts of functional adaptation in populations that are well-founded in molecular evidence, and the cis regulatory element story is weaker in the practical sense that counts most in science (In large part, I think that’s an artifact of the tools — we have better techniques for examining expressed sequences, while regulatory elements are hidden away in unexpressed regions of the genome. Give it time, the cis proponents will catch up!)

This morning, I was sent a nice paper that describes a pattern of functional change in an important molecule — there is absolutely no development in it. It’s a classic example of an evolutionary arms race, though, so it’s good that I mention this important and dominant side of the discipline of evolutionary biology — I know I leave the impression that all the cool stuff is in evo-devo, but there’s even more exciting biology outside the scope of my tunnel vision. Also, this paper describes a situation and animals with which I am very familiar, and wondered about years ago.

[Read more…]

Amphioxus and the evolution of the chordate genome

Blogging on Peer-Reviewed Research

This is an amphioxus, a cephalochordate or lancelet. It’s been stained to increase contrast; in life, they are pale, almost transparent.

i-56ee51e328b10451feb168cd9bab0ea5-amphioxus.jpg

It looks rather fish-like, or rather, much like a larval fish, with it’s repeated blocks of muscle arranged along a stream-lined form, and a notochord, or elastic rod that forms a central axis for efficient lateral motion of the tail…and it has a true tail that extends beyond the anus. Look closely at the front end, though: this is no vertebrate.

i-e961343b9bf5b6dfd74823fba6deeafb-amphioxus_closeup.jpg

It’s not much of a head. The notochord extends all the way to the front of the animal (in us vertebrates, it only reaches up as far as the base of the hindbrain); there’s no obvious brain, only the continuation of the spinal cord; there isn’t even a face, just an open hole fringed with tentacles. This animal collects small microorganisms in coastal waters, gulping them down and passing them back to the gill slits, which aren’t actually part of gills, but are components of a branchial net that allows water to filter through while trapping food particles. It’s a good living — they lounge about in large numbers on tropical beaches, sucking down liquids and any passing food, much like American tourists.

These animals have fascinated biologists for well over a century. They seem so primitive, with a mixture of features that are clearly similar to those of modern vertebrates, yet at the same time lacking significant elements. Could they be relics of the ancestral chordate condition? A new paper is out that discusses in detail the structure of the amphioxus genome, which reveals unifying elements that tell us much about the last common ancestor of all chordates.

[Read more…]