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!
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!