Wednesday, August 1, 2012

Em summarizes

Obbard et al. 2009 Quantifying adaptive evolution in the Drosophila immune system. PLoS Genetics.

Stephen said to read this a while ago, I did, and didn't think much of it. Now, after banging around calculating alpha myself, it seems a lot more interesting ...


Population genetics studies have found that a surprisingly large proportion of changes in Drosophila genomes were fixed by positive selection (this value is measure as α). Obbard and co. explore this result by investigating sequence of immune-related genes, which they expect to have higher rates of adaptive evolution. They resequenced 136 immune genes and 136 nearby non-immune related control genes in 6 populations of Drosophila melanogaster and 2 populations of D simulans, with 4 individuals pooled per population. They first found that, as expected, α is higher in immune genes (α = 0.65) compared to their controls (α = 0.41). Second, they looked at the distributions of α values and found that this difference is driven by a small subset of their immune-related genes. Third, they classified genes by various pathways and function and found that some of these groups have higher average α values than others (this presumably makes sense for people that understand Drosophila immune systems). Finally, they look at lineage specific divergence and show that a values are correlated in D. simulans and D. melanogaster, suggesting that similar selective pressures are operating in both species. 

Overall this paper suggests that, since α is higher in genes that are expected to be under strong positive selection, high α estimates in Drosophila represent reality, not artifacts of some other process. Also interesting, for me, is their calculations of the exact number of variants fixed by positive selection (a), which I'd like to do with my own data. Also, they appear to calculate lineage-specific divergence by using PAML to estimate the ancestral state and then calculate divergence between the inferred ancestor and their sequenced genes, something which the author of PAML says not to do. 

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