If a trait is being selected for, the alleles with large positive effects will compound with a faster growth rate than those with small effects (even if there are initially many more small-effect alleles) and tend to account for a large portion of the heritability of that trait (at least until they have almost swept the population).
You suggest that psychological traits such as personality and cognition have been subject to recent positive selection, so why haven’t GWAS (or targeted investigations, e.g. microcephalin) found much in the way of common large effect alleles for psychological traits? What are your best guesses on the genetic architectures of personality and cognition?
There have been some (tentatively) identified like the 7-repeat
version of the D4 dopamine receptor, the serotonin transporter, and
others that Greg will be able to dredge up from his memory.
We may have found others but not identified them. Imagine that it
would be highly beneficial to have a little bit less of substance s. If
so then a mutation that broke the gene producing s would be favored
a lot and would sweep until people with two copies of broken s
started being born. How likely is it now that two broken copies of s
will still work? A lot of the sweeps identified from SNP scans seem
to have stalled out at intermediate frequencies (as opposed to going
to fixation) suggesting that heterozygote advantage is widespread.
If so the genome wide association studies ought to find them, and
they find a lot, many of the findings are not replicable. So after all
the above I have no coherent answer to your question!
If a trait is being selected for, the alleles with large positive effects will compound with a faster growth rate than those with small effects (even if there are initially many more small-effect alleles) and tend to account for a large portion of the heritability of that trait (at least until they have almost swept the population).
You suggest that psychological traits such as personality and cognition have been subject to recent positive selection, so why haven’t GWAS (or targeted investigations, e.g. microcephalin) found much in the way of common large effect alleles for psychological traits? What are your best guesses on the genetic architectures of personality and cognition?
Yikes! This is worse than my PhD orals.
There have been some (tentatively) identified like the 7-repeat version of the D4 dopamine receptor, the serotonin transporter, and others that Greg will be able to dredge up from his memory.
We may have found others but not identified them. Imagine that it would be highly beneficial to have a little bit less of substance s. If so then a mutation that broke the gene producing s would be favored a lot and would sweep until people with two copies of broken s started being born. How likely is it now that two broken copies of s will still work? A lot of the sweeps identified from SNP scans seem to have stalled out at intermediate frequencies (as opposed to going to fixation) suggesting that heterozygote advantage is widespread.
If so the genome wide association studies ought to find them, and they find a lot, many of the findings are not replicable. So after all the above I have no coherent answer to your question!