Parasitic sex cells wtf yay?

I’m reading a review about asexual reproduction in colonial sea squirts (Brown and Swalla, 2012). This isn’t really the place I expected to stumble on something that made me giggle and whisper “holy fuck” at the same time, but I was totally wrong. Apparently, some squirt colonies can fuse and create a single “chimaera” colony. And then one member’s germ cells can take over the other’s gonads. Because these squirts keep some germ cells in their blood, so they can go wherever the hell they want in the whole colony. Like that poor sod’s testicles.

It seems everything remotely related to sex in the animal kingdom is at least a little bit kinky.

Also, sea squirts are weird, and this is Captain Obvious speaking.

(Must resist temptation to immediately dive into PubMed for articles on germline parasitism. I have a ton of reading to do that’s actually relevant to my work…)

(P.S.: I wonder if tagging this post “sex” will trigger a giant traffic spike. Consider this an experiment!)

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Reference:

Brown FD, Swalla BJ (2012) Evolution and development of budding by stem cells: ascidian coloniality as a case study. Developmental Biology 369:151-162

DNA vs proteins – I learn something again…

If you want to use molecular sequences to uncover the relationships between organisms, you have two choices of molecule. You can use either DNA or the proteins it encodes. I always thought, why the hell would anyone use DNA when they can also use protein?

The DNA alphabet has four different letters, versus the 20 amino acids proteins are made of. There is much more danger of a chance similarity, there’s much more chance of multiple mutations at the same spot returning to the ancestral state and completely erasing important phylogenetic information. You could, I suppose, use codon-based models instead of single-nucleotide models, but what’s the point when you can just translate the sequence and analyse the protein instead?

Well, it seems there is a point. The crucial thing is that while DNA translates unambiguously to protein, this is not true the other way. Take a look at the genetic code table below (modified from here):

The letters in black represent RNA bases (the DNA would have T instead of U), and the coloured ones are the three-letter abbreviations of amino acids, except for Stop, which, as you might have guessed, means “end of protein, stop translating”.

The first thing to note about the table is that most amino acids are encoded by more than one DNA/RNA codon. There’s already more information here than if you simply took the protein sequence. The second point is that some amino acids have two sets of codons that aren’t easily interchangeable.

With something like glycine (bottom right box), all codons are almost the same, only differing in the third letter, which might even be irrelevant anyway due to third base wobble. Mutating between glycine’s codons is easy and unlikely to screw the organism.

In contrast, serine (red and yellow boxes) has two sets of codons that differ in both their first and second positions. It’s much easier to move within either of those sets by mutation than to jump from one set to the other. Changing either of the first two letters in any of these six codons results in a different amino acid, which has a lot more potential to wreak havoc than a mutation that leaves the protein alone.

And apparently, that can, from a phylogenetic point of view, practically turn serine into two different amino acids. In a fairly recent Nature paper, Regier et al. (2010) investigated arthropod relationships and found that while protein-based methods gave very similar results to DNA-based methods, they often couldn’t offer as much support for these results as DNA did. That paper hints at the serine problem and that a couple of the authors are working on it, and now the “working on” bit is out in PLoS ONE. (That’s how I came across this issue, in fact.)

The new analysis (Zwick et al., 2012) finds that tweaking protein-based evolutionary models so that the two kinds of serine count as different letters increases confidence in the resulting tree dramatically. The serines aren’t changing any major conclusions – if you take them out, you still get the same tree, just with lousy statistical support. But clearly, protein sequences alone were missing important evidence. In another situation, they might make the difference between a wrong answer and a right one.

(Now I wonder if anyone’s done codon-based Hox gene phylogenies. Hox genes/proteins can be really difficult to classify because only a short region can be compared among all of them, and this short region evolves pretty slowly, yielding very few informative differences. But what if there’s more information hiding in the codons? There’s not an awful lot of serine in homeodomains, though, and while the other sixfold degenerate amino acid (arginine) is pretty common in them, that one doesn’t have nearly the mutational chasm that separates the two codon clusters for serine. Meh. Maybe codons wouldn’t help at all with Hoxes.)

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*OK, technically, you sort of have three choices, but RNA and DNA sequences contain the exact same information, so they don’t really count as different.

***

References:

Regier JC et al. (2010) Arthropod relationships revealed by phylogenomic analysis of nuclear protein-coding sequences. Nature 463:1079-1083

Zwick A et al. (2012) Resolving discrepancy between nucleotides and amino acids in deep-level arthropod phylogenomics: differentiating serine codons in 21-amino acid models. PLoS ONE 7:e47450

Only so many ways

In a way, the limitations of evolution are more interesting to me than its possibilities. It’s cool to figure out how exquisite adaptations and fantastically complex molecular machines might have evolved, but I like my evolution the way Brandon Sanderson likes his magic. If it can do anything, then where’s the fun? Deep underlying rules and constraints are what make it really interesting.

Convergent evolution can hint at such rules. Some of them are just physics and seem pretty straightforward. If you’re a creature swimming in the sea, being streamlined is good for you, and there aren’t that many ways of being streamlined. So dolphins, squid and sharks have the same basic shape despite coming from very different ancestors. Other cases involve more subtle and probably more interesting constraints. The baggage of your ancestry, the interactions in your genome, the pool of available mutations, can all restrict the ways in which you can adapt to a particular challenge. A study I found in the huge backlog of random pdfs on my desktop probes tentatively into the importance of such intrinsic limitations.

Conte et al. (2012) asked a seemingly simple question that has apparently never been systematically investigated before: how often does convergent or parallel evolution of the same trait result from modification of the same genes?

Convergent and parallel evolution are sort of two ends of a continuum. We use parallel evolution to refer to traits that evolved in similar directions starting from the same starting point. For example, three-spine sticklebacks repeatedly lost their bony armour when they moved from the sea to rivers and lakes in various places around the world. The ancestor is the same heavily armoured marine fish in each case, and most freshwater populations underwent very similar changes (including their genetic basis) from this common beginning. At the other end of the scale you find clear instances of convergence, such as “milk” in mammals and birds. Their common ancestors not only didn’t ooze custom-made immune-boosting baby food, they likely didn’t even care for their young.

Back to the paper. Conte et al. conducted what we call a meta-analysis: collecting and analysing data from all published studies that fit their pre-determined set of criteria. Altogether, they looked at a carefully selected set of 25 studies about the genetic basis of convergent traits. Not too great, the authors acknowledge, but it’s a start.

The studies were divided into two sets, because the two main methods of looking at the genetic basis of a trait can’t easily be analysed together. The first set contained genetic mapping studies (“which parts of the genome cause X?”), and the second candidate gene studies (“does this gene cause X?”). The convergent traits in these studies were quite diverse. There was pale skin from cave fish to humans, African and European peoples’ ability to digest lactose as adults, resistance to tetrodotoxin in snakes, wing patterns in butterflies, electric organs in fish…

The comparisons span quite a long time scale. On one end, there are populations within a single species, like lactose-tolerant Europeans and Arabs, that diverged mere tens of thousands of years ago. On the other, pale-skinned cave fish and Swedes are separated by something on the order of 400 million years. This is part of what makes this an exciting study, because you can indirectly observe what happens to genetic constraints over time.

The most exciting, though, is the sheer amount of gene re-use the researchers saw. For mapping studies, they found a 32% chance that the same trait will be associated with the same gene(s) in different species. Candidate genes give an even higher estimate (55%), but that might just be the nature of the beast. When a candidate gene is not behaving as expected it’s probably less interesting and publishable, Conte et al. argue, whereas mapping studies will usually throw up something to write about.*

Within a species, the probability of the same gene being used in the same adaptation gets as high as 80% for both methods. This is despite the fact that often the traits in question are controlled by several genes, any of which could be mutated to the same effect. Where you come from clearly has a huge impact on where (and how) you can go. The impact lessens as you look at increasingly distant species; at a hundred million years of divergence, mapping data show only 10% similarity between convergent traits, and even candidate genes drop to around 40%. (Methinks 10% is still a big number considering how many genes we have, but of course we’re talking about relatively simple traits here, so the number of relevant genes isn’t nearly as high.)

There are some logical possible explanations behind both the high level of genetic convergence in close relatives and the big drop with increasing divergence. For example, it could be that populations within a species have very similar pools of genetic variation. If the same genes vary, then natural selection will “naturally” hit on the same genes when adaptation becomes handy. It’s also likely that the rest of the genome plays a part – closely related populations/species have more similar genetic backgrounds, their genes likely interact with one another in more similar ways, ergo the restrictions on what mutations can become beneficial are also similar. As lineages diverge, so do such interactions and restrictions, lowering the probability that two species evolve the same trait in the same way.

Of course, it’s at this point impossible to say which of the potential reasons actually cause the trends observed in this study, but that wasn’t the point. The authors’ stated goals were pretty modest:

“[O]ur aim here has been to stimulate thinking about these issues and to move towards a quantitative understanding of repeated genetic evolution” (p5044)

In that, I hope, they have succeeded. It’d be lovely to see more of this “big picture” discussion of convergent evolution. Big pictures make Mammals happy.

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*I’m not sure about that, myself. I think if you’ve got a gene that’s been shown to do X in species after species, a negative finding is a lot more newsworthy than yet another confirmation of the same old shit. I suppose it’s gut feeling versus intuition until someone does a study of that, though 🙂

***

Reference:

Conte GL et al. (2012) The probability of genetic parallelism and convergence in natural populations. Proceedings of the Royal Society B 279:5039-5047

Neurulating acorn worms, and the Mammal is confused

To the everyday animal lover, acorn worms have few things going for them. They are pretty hideous as a rule, and they don’t really do anything interesting. (If you count “eating mud all day” as interesting, you are probably a sediment ecologist…)

True to their mud-eating selves, though, acorn worms are great at muddying the water in the evo-devo world. You see, there’s this neat idea that goes back to the early 19th century called dorsoventral inversion. French naturalist Étienne Geoffroy Saint-Hilaire once noted that an arthropod looks rather like an upside down vertebrate in many ways. This diagram from the Wikipedia entry illustrates the concept rather nicely:

The pink and snot-green triangles on the side represent the expression levels of the key genes that determine where the back and belly sides go. dpp (decapentaplegic) is the fly homologue of BMP4 (or BMP2, 4 and 7, to be precise), and sog (short gastrulation) is the fly version of chordin. So not only do major structures like the central nervous system develop on opposite sides of the body, the developmental genetics are also upside down. It seems like a no-brainer. (Well, chordates had to somehow move the mouth back to the belly side, but hey, no big deal ;))

Then those evil acorn worms come in and complicate things.

Acorn worms belong to the phylum Hemichordata. Hemichordates are most closely related to echinoderms like sea urchins. Together with chordates (vertebrates, sea squirts and lancelets), they make up the deuterostomes. Fruit flies and most worms that aren’t “acorn”, on the other hand, are protostomes.

Whether acorn worms and other hemichordates have a central nervous system at all has been the subject of some debate. Recent evidence suggests that they do (Nomaksteinsky et al., 2009). They don’t even just have one, they have two of them, taking the form of nerve cords on the dorsal and ventral sides of the animal. The dorsal nerve cord forms in a way eerily similar to our own spinal cord. Chordates like ourselves undergo a process called neurulation, in which some of the ectoderm (“skin”) on the embryo’s back folds inwards to form a hollow tube that’s the precursor of the central nervous system. Well, look what happens in an acorn worm (figure from Luttrell et al., 2012):

The left side of this image depicts the process in the acorn worm Ptychodera flava (and shows you a young worm – innit cute?), while the right side illustrates what happens in a chick embryo. (I’m not sure why they didn’t use actual photos of chick neurulation, I don’t imagine they’d be very hard to come by…)

In chordates, the notochord (precursor of our spine) sends out chemical signals to direct nerve cord formation. Acorn worms don’t have anything notochord-like at the time the nerve cord develops, but somehow they make it look like neurulation anyway. If it looks like a duck (or chick, as the case may be) and quacks like one, it might just be one.

The problem?

It happens on the wrong side. Having read the two papers I’ve cited so far, my impression is that neurulation only happens with the dorsal cord. However, in other respects these animals share the arthropod, not the vertebrate, orientation. Most importantly, their genetic dorsoventral axis is oriented like that of arthropods and other protostomes, with BMP levels in the embryo highest on the dorsal side (Lowe et al., 2006). Chordate embryos can’t even make a nervous system at high BMP levels!

It seems that whatever happened to turn the ancestral bilaterian on its head, it wasn’t as simple as flipping the animal and relocating the mouth. The development of the central nervous system shares serious developmental genetic similarities among deuterostomes like us and protostomes like flies (Arendt and Nübler-Jung, 1999) or ragworms (Denes et al., 2007), indicating that if not a full-blown CNS, then at least the genetic pattern was present in our common ancestor.

The figure above is a schematic comparison of gene expression in the developing nervous systems of fruit flies (Drosophila), ragworms (Platynereis) and vertebrates from Denes et al. (2007). The diagram labelled Enteropneust illustrates the lack of data from acorn worms, which I don’t fully understand given that Lowe et al. (2006) actually studied several of the genes included in this figure. Speaking of that, acorn worms once again prove to be weird and confusing, since the genes in question aren’t expressed in anything like the longitudinal stripes seen in the other animals. In fact, Lowe et al. (2006) found that they aren’t obviously associated with either of the nerve cords.

To be precise, Lowe et al. worked under the assumption that acorn worms had no nerve cords, but if you look at their pictures the lack of resemblance is blindingly obvious. For example, Msx, the light grey gene on the Platynereis and vertebrate diagrams, goes all around acorn worm embryos in a relatively narrow ring. Nk2.2, the red gene, isn’t even expressed in the ectoderm (the embryonic “skin”), whereas central nervous systems invariably come from there. Did Lowe et al. get the wrong genes or what? Don’t think so, Msxes at least are pretty easy to recognise…

To summarise: acorn worm central nervous systems develop much like ours, but on the wrong side of the body, with none of the genetic similarities we share with animals much less closely related to us than acorn worms. To top that, the damn worms have another nerve cord on the opposite side, which doesn’t develop by neurulation unless I’ve misunderstood something.

I… have no idea what’s going on here. Damn you, nature, you need to work on your clarity.

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References:

Arendt D & Nübler-Jung K (1999) Comparison of early nerve cord development in insects and vertebrates. Development 126:2309-2325

Denes AS et al. (2007) Molecular architecture of annelid nerve cord supports common origin of nervous system centralization in Bilateria. Cell 129:277-288

Lowe CJ et al. (2006) Dorsoventral patterning in hemichordates: insights into early chordate evolution. PLoS Biology 4:e291

Luttrell S et al. (2012) Ptychoderid hemichordate neurulation without a notochord. Integrative and Comparative Biology 52:829-834

Nomaksteinsky M et al. (2009) Centrarlization of the deuterostome nervous system predates chordates. Current Biology 19:1264-1269

Men in science

Yet again, the BioEssays editor in chief writes something that reinforces my incipient fangirlhood for him. His latest editorial titled Men in Science raises an important point that I think people concerned about gender equality often forget. Equality goes both ways.

If you read that title you might expect a misguided “what about the menz” screed, but that’s not what it’s about, at least I don’t think it is. Moore suggests that in focusing on the difficulties women in science face, we tend to forget that male stereotypes affect these just as much as female stereotypes do. It’s great to fight for, say, women’s right and ability to be both mothers and scientists, but what about men who wish to be fathers and scientists? Wouldn’t it help both men and women in science if they could take time off for their families without serious consequences (be they material or social)? Plus at the top levels, the people making important decisions are overwhelmingly male, ergo the system can’t really be improved without targeting men.

And this is quite in line with the opinion I’ve come to after a lot of reflection. Women’s equality doesn’t just mean that they are free to become like men. It also means that girly girls are not subtly despised, and neither are girly guys. Because while you make fun of guys’ makeup, while you find it strange that dad would stay home with the kids while mum works her arse off to feed them, what you are doing is putting down traditionally feminine things just like the finest of bigots.

Believe me, that was a difficult perspective for me to accept. I love science and maths, wear more bruises on any given day than I wear makeup in a decade, and want nothing to do with motherhood or the colour pink. Nonetheless, I am the product of a society that expects girls to be girly while belittling them for it. Of course it would be difficult not to laugh at the idea of a perfectly normal guy with painted nails, cooking dinner for his hard-working wife with a toddler tugging at his track bottoms.

Yet if I do, am I not perpetuating the very same prejudices I rebelled against?

Time before time?

Pretty much anything that ever sees the sun goes through regular daily rhythms governed by the cycle of light and darkness. Humans tend to sleep at night and be more active during the day (students may not be quite human :-P). Many planktonic organisms feed near the ocean surface at night and migrate to greater depth to avoid predators during the day. External factors like light set the clock, but the cogwheels are the so-called clock genes. Clock genes such as Period and Bmal form an interacting network that results in each gene going through cycles of activity, which ultimately translates to the more obvious changes in physiology and behaviour that we see.

Or at least that’s the traditional wisdom. I came across this study today that challenges the role of clock genes, at least in the rather artificial environment of a stem cell culture. Paulose et al. (2012) used embryonic stem cells from mice to find out when the clock starts ticking. Their hypothesis, based on previous stem cell studies, was that it remains silent so long as the cells remain in a stem cell state. They expected daily rhythms to appear when the cells started differentiating.

Which is not quite what they found. The clock genes whose activity they measured did indeed begin cycling only when they let the cells differentiate. In undifferentiated stem cells, their expression was either absent or irregular. However, the stem cells’ metabolism went through cycles even when the scientists chemically prevented them from differentiating. They took up more glucose at certain times of the day than others, and they made more of a certain glucose-transporting protein at these times. The rhythm became like ten times stronger when the clock genes started working, but it was there even without them.

Now (disclaimer!), I didn’t read the study in detail, but on the face of it I find its results really interesting. It’s as if mammalian cells have several ways of keeping time. Why? Isn’t one enough? And how exactly do the stem cells achieve a rhythm if it’s not through the usual avenues? Are we going to discover another clock network? And, importantly, is this something that happens in real intact embryos, or only in stem cells living in a dish?

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Reference:

Paulose JK et al. (2012) Towards the beginning of time: circadian rhythms in metabolism precede rhythms in clock gene expression in mouse embryonic stem cells. PLoS ONE 7:e49555

Birds invent the password!

This is quite outside my normal favourite topics, but it’s so cool I had to share anyway. (Though I guess it’s still not quite as far outside as, say, exoplanets :D)

A study of nesting superb fairy wrens (Colombelli-Négrel et al., 2012) suggests that these beautiful little birds use something akin to a password to defend against cuckoo infiltration. While the female sits on her eggs, she calls to them. The chicks inside listen, and when they hatch, their begging contains sounds that match a characteristic part of mum’s nesting calls. Learning is clearly going on – when you switch eggs between different nests, the chicks’ cries are most similar to their foster mother’s and not their genetic mother’s calls. (So while the technique might work against cuckoos, it’s no good against cuckoldry ;))

(Superb fairy wrens from Wikipedia. Female (left) by Fir0002/Flagstaffotos, male in breeding plumage (right) by JJ Harrison.)

The female uses the same password to tell her mate to feed her, so he also learns. The crucial thing is that cuckoo chicks don’t. Maybe it’s because they hatch earlier; since female fairy wrens stop making their calls when the first egg hatches, a hatchling cuckoo has had less time to memorise them than a hatchling wren. Either way, both parent wrens can tell the difference. By playing back the begging of wren chicks brooded in the target nest, wren chicks from elsewhere, and cuckoo chicks, the researchers determined that the parents react differently to “home” and “foreign” calls. When the begging cries contain the correct password, they feed the chicks more and spend less time on the lookout for intruders. Interestingly, it makes no difference whether the calls are from another wren nest or from a cuckoo. If you got the password wrong it doesn’t matter if it was by one measly typo 🙂

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Reference:

Colombelli-Négrel D et al., (2012) Embryonic learning of vocal passwords in superb fairy-wrens reveals intruder cuckoo nestlings. Current Biology in press, available online 08/11/2012, doi:10.1016/j.cub.2012.09.025

Beautiful aliens

When you think nature can’t get any more weird and wonderful, count on the deep sea to prove you wrong. Just saw this guy via I fucking love science on Facebook, and wow. What a beauty! (Figure from Lee et al., 2012)

This deep water dish drainer is a harp sponge (Chondrocladia lyra), a newly described member of a group of weird carnivorous sponges. Like so many other creatures at the bottom of the Northeast Pacific, it was captured by the cameras of the Monterey Bay Aquarium Research Institute (here’s the story at MBARI’s own website). Their robotic explorers brought two of the animals to the lab for flesh and blood scientists to take apart and examine in detail, and captured several more on video.

The harp sponge’s slender branches are equipped with tiny hooks that capture small crustaceans for the sponge to engulf and digest. At the branch tips, sperm is made in those little bulbs and then released into the water. The prey-catching snare of branches also intercepts sperm, and it seems that this might trigger the maturation of eggs in the recipient (Lee et al., 2012). Making eggs only when you’ve got hold of some quality sperm is a nice way of conserving energy in a notoriously resource-poor environment!

(… and I think the creature looks totally Ediacaran, even if it doesn’t really resemble any particular Ediacaran fossil. Don’t ask how I make these associations 😛 Either way, it’s gorgeous!)

Incidentally, I was googling for images of other Chondrocladia species, and quite unexpectedly I stumbled on a lovely piece of art inspired by one. This might be even cooler than space Anomalocaris:

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Reference:

Lee WL et al. (2012) An extraordinary new carnivorous sponge, Chondrocladia lyra, in the new subgenus Symmetrocladia (Demospongiae, Cladorhizidae), from off of northern California, USA. Invertebrate Biology early view, available online 18/10/2012, doi: 10.1111/ivb.12001

Something of a misnomer…

Nature has a way of screwing with the human desire for order and simplicity. One of the most egregious examples I’ve encountered is the contrast between what you learn about animal development and, well, reality.

Bilaterian animals have been traditionally divided into two great groups: protostomes and deuterostomes. If I whip out my trusty little animal phylogeny, deuterostomes are indicated right there in the middle, and protostomes are the sum of the ecdysozoans and lophotrochozoans. (Whoever came up with the latter name, urgh. I have to think twice before I say or type it, and I’ve been into them for years.)

The names “protostome” and “deuterostome” were nicked from ancient Greek and literally mean “first mouth” and “second mouth”. They refer to where the mouth comes from during the development of these animals. Animal embryos go through a process called gastrulation, during which the initially ball- or disc-like embryo folds in to form a pocket, the primitive gut or archenteron. The archenteron connects to the outside through a single hole, the blastopore. In protostomes, supposedly, the mouth comes straight from the blastopore, hence “first mouth”. In deuterostomes, the blastopore forms the anus while the mouth opens somewhere else. (Or that’s what they teach you at school anyway)

Here’s a really cool animated gif of gastrulation in sea urchins from Stanford University’s sea urchin embryology resource. Note how the mouth appears late in the process and joins up with the archenteron – sea urchins are good and proper deuterostomes! (The red dots are the cells that form the larval skeleton, in case you wondered)

And here are real sea urchin embryos before and during gastrulation (source):

(Sea urchins are neat.)

That sounds nice and simple and clear-cut, which should be a big warning sign that it’s too neat to be true. As far as I know, deuterostomes are relatively well-behaved in this respect, but protostomes… protostomes are horribly misnamed. Hejnol and Martindale (2009) compiled a table of what’s known about the various openings in different bilaterian phyla, and found protostomes to be all over the place. In protostome embryos, the blastopore may become the mouth, the anus, both or neither, and this often varies even within a phylum.

In Hejnol and Martindale’s book chapter, priapulids (a. k. a., and I’m not kidding, penis worms) are listed as “?blastopore closure”. Well, when Andreas Hejnol and friends looked more closely at priapulid embryos, that became “nope, definitely deuterostomy”. Not only does the priapulid blastopore become an anus, its surroundings also express genes associated with butthole formation, and the “mouth” genes are active on the opposite side of the embryo. (Below: Priapulus developmental stages, from Martin-Durán et al. [2012] The forming mouth [mo] and anus [an] are marked by shiny green concentrations of actin protein.)

That’s not just another addition to an already long list of deuterostomous protostomes, the study argues. Priapulids are considered to be one of the more conservative phyla among the ecdysozoans. With nematodes for comparison that’s not saying much, but this study suggests that they are quite conservative in terms of gut developmental genetics. The authors also note that deuterostomy was likely the ancestral condition for both nematodes + nematomorphs and arthropods + water bears + velvet worms (I’m not sure how strong that inference is based on what they write about the above groups). That means it’s likely to have been the way the last common ancestor of ecdysozoans developed. Given that deuterostomes are deuterostomous, the ancestral ecdysozoan probably was, and arrow worms, a weird ?protostome phylum that’s probably neither ecdysozoan nor lophotrochozoan, also are, this seems to suggest that all bilaterians came from a deuterostomous ancestor. (Below: the front end of an arrow worm, just for the heck of it. Yvan Perez, Wikimedia Commons.)

And that speaks against one of the more popular theories on how bilaterians came about from a jellyfish-like ancestor. Cnidarians such as jellyfish and coral polyps have only one gut opening, which is derived from the blastopore. A popular (and, IMO, quite appealing) idea is that this opening elongated in the ancestors of bilaterians, and separate mouths and anuses came from the long slit-like blastopore closing in the middle. If the last common ancestor of bilaterians is shown to be deuterostomous, this proposition remains without evidence.

There’s always a catch, though. Remember what I (or rather, Hejnol and Martindale) said about variation within phyla? Well, priapulids today are not the most diverse phylum to put it mildly, but there are still sixteen known species in two extant classes. Martin-Durán et al. (2012) examined one. You know the obvious question: how do the others develop?

It occurs to me that with so few living species, priapulids are among the few phyla for which this question could be answered completely 😀

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References:

Hejnol A & Marindale MQ (2009) The mouth, the anus, and the blastopore—open questions about questionable openings. In: Telford MJ & Littlewood DTJ (eds.) Animal Evolution: Genomes, Fossils and Trees. Oxford University Press, pp. 33-40

Martin-Durán JM et al. (2012) Deuterostomic development in the protostome Priapulus caudatus. Current Biology in press, available online 25/10/12, doi: 10.1016/j.cub.2012.09.037