Friday, December 02, 2005

Skin color loci - older work   posted by Razib @ 12/02/2005 08:10:00 PM

About two months ago I posted an entry where I sketched out an extremely simple model for skin color assuming there were 6 loci and two alleles (on and off). There was a reference in the comments to "5 loci" for skin color as a quantitative trait. From what I can gather that assumption derives from a paper published in 1981 by Russ Lande, which is online. In reality that paper simply draws upon older work from 1964, and its primary focus is on estimating the number of loci in crosses between heterogenous populations (using inbred lines was the way pioneered by Sewall Wright). But, it turns out that Cavalli-Sforza and Bodmer discuss that older work in Genetics of Human Populations, which I have a copy of. Today genomics is exploring the details of the loci which control for skin color, but we have a long way to go, so I'm going to reproduce some of the data and conclusions from Bodmer & Cavalli-Sforza's work so that it will be online....

Table 9.6
Means and Variances of Skin Color Measurements
Antilog of (Reflectance at 685 mμ) for Various Matings

Population - No. of Observations, Mean, Variance (X 1000)

Caucasian - 105, 0.421, 1.09
Negro - 106, 0.225, 1.05
F1 - 94, 0.334, 1.59
Negro backcross - 26, 0.304, 1.71
Caucasian backcross - 30, 0.382, 2.00
F2 - 14, 0.346, 1.99

FYI, an F2 is simply F1 X F1, explaining the small sample size. By analyzing the means they concluded there was no "dominance effect." The hybrid individuals tended to have skin reflectance measurements about midway between their parental values. An analysis of the variance yielded the number of loci as 4, but, this was subject to a very high error. Nevertheless, 4 is probably the low bound, as these analyses usually underestimate the true number. But, they often capture the essential gist because for many traits a small number of genes determine most of the variation on a trait (the traditional assumption, reflected in Plomin's work, is that IQ is different in that there isn't much with more than 1% effect, though Greg and Henry's Askhenazi work are starting to puncture that preconception). The genetic data coming out right now suggests that contrary to the implication in the model above (stated explicitly in the text) Europeans are not fixed for a particular allele on many of genes (i.e., MC1R). But, the phenotypic outcome of "loss of function" mutations is basically the same, so in terms of quantitative traits I think you can ignore the lack of identity by state on the nucleotide level.

Notes: They took the antilog to adjust for scaling effects, didn't matter anyhow. Additionally, I left the text as is aside from reformatting some of it, so sorry about the use of words like "Negro" if you are offended, it was 1971.