Common elements of eumetazoan gene organization in an anemone

We now have a draft of the sea anemone genome, and it is revealing tantalizing details of metazoan evolution. The subject is the starlet anemone, Nematostella vectensis, a beautiful little animal that is also an up-and-coming star of developmental biology research.

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(click for larger image)
Nematostella development. a. unfertilized egg (~200 micron diameter) with sperm head; b. early cleavage stage; c. blastula; d. gastrula; e. planula; f. juvenile polyp; g. adult stained with DAPI to show nematocysts with a zoom in on the tentacle in the inset; h, i. confocal images of a tentacle bud stage and a gastrula respectively showing nuclei (red) and actin (green); j. a gastrula showing snail mRNA(purple) in the endoderm and forkhead mRNA (red) in the pharynx and endoderm; k. a gastrula showing Anthox8 mRNA expression; l. an adult Nematostella.

A most important reason for this work is that the anemone Nematostella is a distant relative of many of the animals that have already been sequenced, and so provides an essential perspective on the evolutionary changes that we observe in those other organisms. Comparison of its genome with that of other metazoans is helping us decipher the likely genetic organization of the last common ancestor of all animals.

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Mrs Tilton is back…forever!

She’s fired up the The Sixth International again, and she threatens promises to be at it for a long, long, long time—she bears a longevity mutation, a single nucleotide substitution in the mitochondrial genome associated with some long-lived people. And some people claim there is no such thing as a beneficial mutation…

Anyway, it’s personally interesting that it’s mitochondrial—that means it is passed down through the maternal line. Since my father’s side of the family is grievously short-lived, but my mother’s side keeps going for nearly forever, that’s good news, if the maternal secret is particularly robust mitochondria. Since this particular allele appears in various lines all around the world, there’s a slim chance.

Otherwise, I’m afraid my only mutant power seems to be the ability to dissolve chewing gum. I was ripped off.

Pair-rule genes

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The general pattern of developing positional information in Drosophila starts out relatively simply and gets increasingly complicated as time goes by. Initially, there is a very broad distribution of a gradient of a maternal morphogen. That morphogen then triggers the expression of narrower (but still fairly broad) bands of aperiodic gap genes. The next step in this process is to turn on sets of genes in narrow, periodic bands that correspond to body segments. This next set of genes are called the pair-rule genes, because they do something surprising and rather neat: they are turned on in precisely alternating bands. In the picture above, for instance, one pair-rule gene, even-skipped, has been stained blue, and it is expressed in parasegment* 1, 3, 5, 7, etc. Another, fushi tarazu, has been stained brown, and this gene is turned on in parasegments 2, 4, 6, 8, etc.

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An almost biblical curse

There are a couple of small towns on the border between Utah and Arizona that are basically feudal theocracies, ruled by a particularly nasty splinter sect of polygamist Mormons. It’s got some truly ugly social consequences — daughters are prizes given away to church leaders, while sons are competitors who are driven away — but now it turns out that there also some biological consequences. The community is deeply inbred, and their prize is the possession of the highest rate of fumarase deficiency in the world, with at least 20 afflicted children in the last 15 years. Fumarase is an enzyme in the Krebs cycle; deleterious mutations in these genes cause a metabolic disorder called fumarase deficiency.

It’s not a nice innocuous disease. It’s variable in its severity, but bad cases lead to debilitating mental retardation, frequent seizures, characteristic appearance (a large head, coarse features), and death. With care, affected individuals can live for many years, but they’ll never be self-sufficient and they do require near-constant attention.

And because it is widespread in a small isolated community, that for various reasons (including religion) is neither a desirable destination for new residents nor will its population try to integrate with the outside world, it’s going to get worse. Half the children born to a pair of carriers will be carriers of the disease themselves, and those nice big Mormon families produce lots of children. Not only are the young girls in this community forced to marry and start spawning baby after baby, but compound the horror with the idea that some will be having children who will need to have their diapers changed for 20 years…

Step away from that ladder

We’ve often heard this claim from creationists: “there is no way for genetics to cause an increase in complexity without a designer!”. A recent example has been Michael Egnor’s obtuse caterwauling about it. We, including myself, usually respond in the same way: of course it can. And then we list examples of observations that support the obviously true conclusion that you can get increases in genetic information over time: we talk about gene duplication, gene families, pseudogenes, etc., all well-documented manifestations of natural processes that increase the genetic content of the organism. It happens, it’s clear and simple, get over it, creationists.

Maybe we’ve been missing the point all along, though. The premise of that question from the creationists is what they consider a self-evident fact: that evolution posits a steady increase in complexity from bacteria to Homo sapiens, the deep-rooted idea of the scala natura, a ladder of complexity from simple to complex. Their argument is that the ladder cannot be climbed, and our response is usually, “sure it can, watch!” when perhaps a better answer, one that is even more damaging to their ideology, is that there is no ladder to climb.

That’s a tougher answer to explain, though, and what makes it even more difficult is that there is a long scientific tradition of pretending the ladder is there. Larry Moran has an excellent article on this problem (Alex has a different perspective), and I want to expand on it a little more.

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Wells on Hox structure: making the same mistakes over and over again

Jonathan Wells apparently felt the sting of my rebuttal of his assertions about Hox gene structure, because he has now repeated his erroneous interpretations at Dembski’s creationist site. His strategy is to once again erect a straw man version of biologist’s claims about genetic structure, show that biologists have refuted his dummy, and claim victory. The only real question here is whether he actually believes his historical revisions of what we’ve known about Hox genes, in which case he is merely ignorant, or whether he is knowingly painting a false picture, in which case he is a malicious fraud.

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Wells’ flagrantly false commentary on Hox complex structure

This evening, I am watching an episode of that marvelous and profane Western, Deadwood, as I type this; it is a most excellently compensatory distraction, allowing me to sublimate my urge to express myself in uncompromisingly vulgar terms on Pharyngula. This is an essential coping mechanism.

I have been reading Jonathan Wells again.

If you’re familiar with Wells and with Deadwood, you know what I mean. You’ll just have to imagine that I am Al Swearingen, the brutal bar-owner who uses obscenities as if they were lyric poetry, while Wells is E.B. Farnum, the unctuous rodent who earns the contempt of every man who meets him. That imagination will have to hold you, because I’m going to restrain myself a bit; I’m afraid Wells would earn every earthy sobriquet I could imagine, but I’ll confine myself to the facts. They’re enough. The man completely misrepresents the results of a paper and a whole discipline, and does it baldly on the web, as if he doesn’t care that his dishonesty and ignorance leave a greasy, reeking trail behind him.

Let’s start with Wells’ own words.

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A straightforward example of creationist error

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A creationist, Rob McEwen, left me a little comment here which lists a number of his objections to evolution. It’s a classic example of the genre, and well illustrates the problem we have. The poor fellow has been grossly misinformed, but is utterly convinced that he has the truth. I’m not going to dismantle his entire line of blather (thanks to Loren Petrich, who has already briefly pointed out the flaws in his thinking), but I do want to show what I mean with one example.

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Curing malaria by helping mosquitos

Here’s a clever (I think) observation in the efforts to eradicate malaria: the mosquitos that transmit malaria are also infected with the disease-causing parasite, so maybe if we cure malaria in mosquitos, it will end one intermediate step in the transmission chain. It sounds like a crazy idea, but recent experiments suggest that it might just work. It’s got the advantage of allowing the use of transgenic techniques on the mosquito population, where you don’t have to worry about patient’s rights or whether a few of your experimental subjects will die during the procedure, and you can just let the untreated population wither away and die, and no one can complain. There are a few other ethical concerns, however.

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