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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Basics: What is a gene?

I mulled over some of the suggestions in my request for basic topics to cover, and I realized that there is no such thing as a simple concept in biology. Some of the ideas required a lot of background in molecular biology, others demand understanding of the philosophy of science, and what I am interested in is teetering way out at the edge of what we know, where definitions often start to break down. Sorry, I have to give up.

Seriously, though, I think that what does exist are simple treatments of complex subjects, so that is what I’m aiming for here: I talk a lot about genes, so let’s just step way back and give a useful definition of a gene. I admit right up front, though, that there are two limitations: I’m going to give a very simplified explanation that fits with a molecular genetics focus (pure geneticists define genes very differently), and I’m going to talk only about eukaryotic/metazoan genes. I tell you right now that if I asked a half dozen different biologists to help me out with this, they’d rip into it and add a thousand qualifiers, and it would never get done. So let’s plunge in and see what a simple version of a gene is.

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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.

MADS boxes, flower development, and evolution

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I’ve been writing a fair amount about early pattern formation in animals lately, so to do penance for my zoocentric bias, I thought I’d say a little bit about homeotic genes in plants. Homeotic genes are genes that, when mutated, can transform one body part into another—probably the best known example is antennapedia in Drosophila, which turns the fly’s antenna into a leg.

Plants also have homeotic genes, and here is a little review of flower anatomy to remind everyone of what ‘body parts’ we’re going to be talking about. The problem I’ll be pursuing is how four different, broadly defined regions of the flower develop, and what that tells us about their evolution.

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