Here are the rankings for this year according to Transparency International.

RPM’s slamming of some silly coverage of the C-value enigma got me thinking about the problem of why we see the sorts of variation we do in the amount of non-coding DNA between species. People are right to heckle the questionable assumption that these differences in ncDNA have anything to do with the evolution of phenotypic complexity (though probably a small fraction do), but I think it might still have an interesting functional tale to tell. I’m probably not the first to think of this, but the idea is that variations in quantity of ncDNA are not functional for the organism in themselves but rather the waste product of a particular kind of functional change: gene duplication.

Recall that eukaryotic genomes are regularly bedevilled by selfish tranposons. These are rogue genetic elements with a vested interest in creating duplication events, and the basic idea is that every once in a while one of them will succeed wildly at it and in the process end up dragging a whole gene along for the ride (maybe several times). Most of the time this will be bad, but occasionally it’ll be good, and sometimes it’ll be nearly-neutral and you’ll see functional divergence on the copied locus after the initial duplication event. In the cases where a duplicated gene confers a selective benefit, the newly formed transpositional elements hitchhike along on the newly selected gene’s coattails.

The upshot of this is that we should expect cases of adaptive evolution via gene duplication to be frequently be accompanied by increases in the amount of transpositional cruft in the genome of the species. This also would neatly account for much of the ncDNA variation between species, since gene duplication seems to play an important role in the emergence of species-specific traits. If this idea is correct, the amount of ncDNA should correlate more highly with how much adaptive gene duplication a lineage has undergone rather than phenotypic complexity per se.

This theory should be pretty easy to test: Look at cases of adaptive gene duplication that have happened relatively recently (geologically speaking) and compare the LINEs and such around these loci with those close to the presumed “parent” locus. The further back in time you go the harder it will be to do this comparison due to drift wiping out the traces, but in the cases that are comparable they should have a very similar pattern of nonfunctional repeats. If I have this right. (EDIT: Duh. This isn’t a good test, since you’d probably see the same thing under any sort of duplication. Need to think of something else. Maybe compare lineages of recently duplicated genes: If gene B is a “recent” duplication of gene A, and gene Y is a “recent” duplication of gene X, but genes A and X diverged an extremely long time ago, then the two duplications were probably caused by different retrotransposons and so the LINEs around A and B should tend to be highly similar to each other but very different than those around X and Y, and vice-versa. You’d probably have to compare a bunch of different gene lineages to get a statistically significant result, though, and I don’t know how easy it would be to find enough good candidates.)

Has anyone actually looked at anything like this? Does this idea hang together? How else could we test it?

Update: Looks like another beautiful hypotheses slain by an ugly fact. I’ll just copy-paste what I said in the comments:

Having looked into it, this doesn’t work the way I thought it would. I knew that LINEs sometimes end up dragging some of the host’s genetic material along in their replications, but now I know that the way this happens is that sometimes the reverse-transcription machinery grabs onto host mRNA that’s floating around and splices it in. So what’s being inserted is automatically a pseudogene since the mRNA has already been processed (i.e. there’s no promoter attached to it). For this idea to work it would need to be an active gene. Rats.

Mind you, DNA transposons could still easily easily be a major source of gene duplication since they skip the RNA middleman. But since they’re only a tiny fraction of ncDNA that means it probably has nothing to do with the C-value enigma.

Regular readers know that I often check in on the results from The Barna Group, an evangelical Christian polling outfit. On the one hand I think The Barna Group tends to be a bit alarmist (they have a very narrow definition for a “Biblically based Christian,” e.g., Catholics don’t count), but on the other hand you can be sure that they aren’t going to be pushing atheist wishful thinking. So I was really interested when I saw that a new study had come out, A New Generation Expresses its Skepticism and Frustration with Christianity. In short, the authors find that a growing number of young adults are unaffiliated with Christianity, and many are downright hostile toward the religion. The authors are at pains to point that this is not “just a phase,” a far smaller proportion of Baby Boomers at the same age were religiously skeptical.

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In my post below I respond to Bryan Caplan’s critique of Greg Clark’s claim that disease can increase per capita income because it reduces population (i.e., same population has a bigger resource base to work with).1 I go the route of the two handed economist by suggesting that whether Clark or Caplan is right depends on the details.2 Herrick adds in the comments:

Caplan’s big claim is that almost anything that persistently raises death rates is likely to persistently reduce output per living worker. It that true?

One possible source of persistent increases in death rates that have no impact on productivity: Many kinds of infectious disease.

I’d welcome medically-informed comments on the topic, but it seems possible for infectious disease (from, say the bad sanitation that Clark emphasizes) to raise the chance of dying any given month without appreciably hurting your productivity most of the time.

Scenario: You get sick for a week or two every couple of years, and if you survive, you go back to being productive. If you don’t survive, well then, you’re pushing up the death rate.

As I suggest below I think that Caplan is wrong if he wants to claim that productivity is always decreased in direct proportion to the increased disease load (ergo, death rate) of a population. This would prevent the rise in incomes which Clark predicts as the lower productivity of each individual means that the same amount of land can support fewer people at or above subsistence. In A Farewell to Alms Clark reports a rise in incomes after the Black Death, and, amongst native peoples in the New World after Old World diseases ravaged them. Obviously this is one extreme cause: a highly lethal infectious disease which cuts down a large proportion of the population very quickly, and then recedes. The other scenario is a case where there is an endemic infection which reduces physiological fitness across the whole population, reducing lifespan and increasing death rates, but also dampening economic productivity. Then there are cases where there is a wide variance within the population in regards to susceptibility toward infectious agents. This might be more like the first scenario, a large number of people die very quickly, while many others are spared because of some immunity. And so on.

From Darwinian first principles it seems that there should be a large number of pathogens which are infectious but not fatal. Though reducing physiological fitness, they don’t knock out their host because to do so would result in their own reduced evolutionary fitness. But hey, Herrick asked for expert opinion. I was actually hoping that someone with medical expertise (e.g., tropical diseases?) would weigh in on that thread, but that didn’t happen. So I come to you with open hands and ask you to enlighten….

Update: Greg Clark responds directly to the Caplan critique. As a non-economist I’m more interested in what the empirical historical data says, and what little I know seems to agree with the general thrust of Clark’s point.

1 – That sentence should filter out chimpanzee readers since it should be totally incomprehensible to them.

2 – No shit it depends on the details!

Apropos of a previous post on race, PLoS Medicine has just published two (opinion) articles on the use of racial categories in medicine. There’s only a cursory treatment of genetics (and the treatment that’s there is pretty bad), but it’s sometimes useful to see another take on the issue. The message I get is that, well, doctors aren’t trained in genetics, so any “race-based” medicine (which is necessarily based on probabilites) is likely to become a sort of “black = medicine X, white = medicine Y” dogma.

A note for readers, there’s a new book aimed at the popular audience, Justinian’s Flea: Plague, Empire, and the Birth of Europe. You can find reviews here and here. I’m going to pass on it probably because it is a general interest book which doesn’t introduce any original material, but it looks like some readers of this weblog get something out of it (though do read Plagues and Peoples if this genre is new to you).

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I’m not going to spend too much time on this, but Larry Moran has responded to my post. He, of course, makes it sound as if he’s being perfectly reasonable. But consider what he wrote in July:

[E]volutionary biologists like Dawkins and the other adaptationists should have known about random genetic drift. Isn’t it amazing that they don’t?

And compare with his new line:

There are many adaptationists who recognize that random genetic drift exists. They will, when pressed, admit that neutral alleles can be fixed in a population.

He goes on to dispute that his quotation from Dawkins was misleading. I obviously disagree, because I was misled! When Dawkins writes “If a whole-organism biologist sees a genetically determined difference among phenotypes, he already knows he cannot be dealing with neutrality in the sense of the modern controversy among biochemical geneticists”, I assumed (as most readers likely did) that Dawkins was dogmatically asserting that absolutely no phenotypic change can be neutral. He wasn’t, of course.

In any case, if Moran wants to define an “adaptationist” as someone who hypothesizes an adaptative force driving most phenotypic changes, then sure, Dawkins is probably an adaptationist, as am I and many reasonable biologists. Hypotheses have to be confirmed, of course, and “adaptationism” (tempered with knowledge of demographic forces) is a powerful hypothesis-generating machine. Keep in mind that one of Moran’s “textbook examples” of neutral phenotypes is eye color. OCA2 (the major locus controlling eye color in humans) of course shows one of the strongest signals for selection in the human genome. I have hypotheses about why this is (could be an example of pleiotropy), but if you can just assert that eye color is a neutral character, why even bother?

UPDATE: Larry Moran claims the first of his quotes above was both ironic and sarcastic. Judge for yourself (in his favor, the claim is obviously wrong. in his disfavor, if you weren’t familiar with Dawkins’s writing, it wouldn’t seem obviously wrong). Maybe he means ironic in the Canadian sense.

Bryan Caplan has initiated a series of posts where he will critique some aspects of Greg Clark’s book A Farewell to Alms. Caplan starts by disputing Clark’s implication that the Four Horsemen can increase per capita income simply by reducing population. I would say he makes some good points, but he does leave an opening:

…A plague might do the trick – it kills some outright, and weakens the rest. In the long-run, the survivors will have a higher material level of living. But this hardly makes the plague a “friend of mankind.” All it means is that after mass death, the frail, disfigured survivors will get to eat some extra calories beside the graves of their families. With friends like this, mankind doesn’t need enemies.

The after effects of disease vary quite a bit from pathogen to pathogen and person to person. Additionally, to some extent plague might be a partly exogenous variable, on occasion cutting through populations like a scythe for a few short years and then abating mysteriously for decades. I think this is why the conditions after the Black Death are a good case study which probably leans toward Clark’s contention. 25% of Europe’s population disappeared, but the survivors were not 25% less healthy or productive. In any case, add Econlog to your RSS to keep track of the debate.

Update: Arnold Kling is feeling Clark more than Caplan.