You and Your Genes: Who Wins?

Excellent as usual. Clear, concise and interesting. What a contrast with the usual ID / Creo blogs. Written by one of the (probably) Nial of the Nine Hostages descendents!

Carl --- Ditto what J-dog said.

However, I'm having some difficulty with a human gene only 37,000 years old. Everywhere? Highlands of New Guinea? Australians? Kalahari Bushmen?

I have no difficulty with the gene flow across Europe and most parts of Asia in that length of time, I guess. Just sub-Sahara Africa and otherwise the more remote bits...

David; From my reading, the gene itself is older than 37,000-years-old. Only the most common variation is that young. And it's not quite everywhere...70% of the population, instead.

Ja Kitos --- Thank you. I should have written gene variation. Does your reading indicate just where this variation is absent?

I have trouble with the assignment of (for example) the "mongol" Y-chromosome specifically to Ghengis Khan. Given (1) that the Y-chromosome has extremely low variability and (2) that the mongol conquerors originated in a relatively small area, it's likely that at least some of these men shared male ancestors. I suspect that the y-variant originated before the Khan and that some (much?) of the subsequent spread was perpetrated by his cousins, etc. To attribute all of these Y-chromosomes to one man is to speculate beyond the data.

I have to wonder if it was really Genghis Khan's Y-chromosome, or the Y-chromosome of one of his ancestors. If, for example, Genghis Khan's grandfather had the mutation, and Genghis Khan's empire had a lot of nepotism, then he would've helped his brothers and cousins (who had the same allele) become more successful reproductively speaking. The dates would also allow for that scenario (Genghis Khan was born in 1162, the allele is estimated to have appeared around 1000 AD plus or minus 300 years).

Great stuff, as usual. However, I'd like to say my two penn'orth for the losers.

To be sure, you state that the spread of any particular allele doesn't betoken anything special for its carriers, but there is a flipside -- pure blind luck. Alleles survive, in part, not because they confer any kind of adaptive advantage, but because their competitors die out, a process called random genetic drift. This is a sampling effect and is more prominent in smaller populations than in large ones. Indeed, in very small populations, the effects of drift overwhelm selection.

This is important given the suspicion that for most of human history, populations have indeed been very small. And, I'd go as far as saying that they were even smaller than that, as the key parameter is not gross population size, but something called 'effective' population size -- that is, the segment of the population that actually gets to pass on its genes at all: most organisms die without issue. This isn't to say that selection isn't important, because it is, but only to temper the easy elision that a surviving marker must necessarily have some adaptive advantage, and the elisions that come after that, which always assume a steady, linear progress of man from the apes and up to the angels.

I raise this because of the brouhaha following the 1987 paper by Allan Wilson's lab announcing 'mitochondrial Eve' in Biblical terms, as if the scientists could have identified one woman, the ancestress of us all. Well, maybe so, but Eve was special only because all the other variants of mtDNA which might have existed in Eve's time have died out.

Evolution isn't about progress. It's about the story of those very few organisms -- very few indeed -- that manage to survive the scythe. Or the salmon mousse. You have been warned.

Does your reading indicate just where this variation is absent?

it's not absent anywhere.

a map of the frequency of the derived microcephalin allele in a number of global populations is at the bottom of this post:
http://www.gnxp.com/blog/2005/09/this-is-bruce-lahns-brain-on-aspm-and…

p-ter: Thank you for the link! Reading the comments suggests various errors in the maps. But the places that the variation is rare generally agree with, for example, Stephen Oppenheim, "Out of Eden", Constable & Robinson, 2003, regarding Out of Africa and all that...

Carl Zimmer --- After a bit more checking, I'll opine that this gene variation arose in Southwest Asia, thence spreading both to Europe and across Central Asia to Siberia and the Americas. The frequency elsewhere is low enough to be accounted for by modern interbreedings. But in early times, it appears that gene flow from Europe did not much occur.

It still might have arisen from Neanderthal, as remains are known from at least three locations in Southwest Asia.

If you check out the book Maybe One by Bill McKibbin, he has an intereresting refutation of the idea that your children are "replacements" of you. Most parents have kids in their 20s or 30s and live into their 70s or 80s. A sixty year overlap in lifespans is hardly keeping the population steady.

I'm just sayin.

Thanks for the (as usual) great article.

The microcephalin gene doesn't seem to have done a lot for the survival of the original Neanderthal (?) possessors, who were extinct about 20ky after the transfer. I think we can assume the power of the gene within homo sapiens lies in combination with some other gene/s that had mutated in sapiens after the split from the LCA of sapiens and Neanderthal. As sapiens was already widespread around the world, and with culture, by 43ky ago I doubt the gene impacts on adults. Maybe it assists infant brain development in cold climates? It will be interesting to see what emerges over time.