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closecomments and questions about paper
Posted by scott_p_egan on 16 Jan 2008 at 17:31 GMT
We read this paper in the Vanderbilt E&E student reading group this
week. A very clear, concise paper that got me thinking. I have listed a
couple of questions below that I would appreciate feedback on from
other readers or the authors.
1. Given the age of divergence (13-16MYA), could the lack of fixation
of DMIs suggest non-neutral effects of these mutations within species,
thus selection maintains heterozygosity at these loci?
2. Would a linkage disequilibrium analysis on the AFLP loci showing
segregation distortion be informative? If LD appears high, this might
suggest fewer overall DMI loci and that multiple AFLPs hit the same
gene region; if LD appears low, this might suggest many independent DMI
loci.
3. Given that AFLPs are dominant and DMIs typically result from
recessive mutations in each gene pool, could any inferences be made
from the data on whether locus tied to a DMIs in this study were
dominant or recessive?
Thanks,
Scott Egan
Vanderbilt University
RE: comments and questions about paper
danbolnick replied to scott_p_egan on 26 Jun 2008 at 20:00 GMT
Hi Scott,
In response to your comments:
1) Either the loci involved are neutral and happen to be some of a large number of loci contributing to declining hybrid viability, or they must be under balancing selection. It seems unlikely that they are under positive selection, but distinguishing between these will be tough.
2) These are F1s, so LD won't be informative, except to within a chromosme at best, but given our small sample size even this will be tough.
3) The dominance of the AFLPs won't tell us much about the loci causing hybrid inviability.
A final note: Michael Turelli recently pointed out to me that while the loci we are finding are contributing to hybrid inviability, this does not necessarily make them DMIs in the classic sense. Think of it this way: if we have a normal distribution of some trait affecting health in a species, such that nearly all individuals exceed some threshold for viability. Now, in hybrids, some genes lower their overall health in a way that is the same across all hybrids (full expression of DMIs that reduce vigor, rather than kill). Now, a greater fraction of individuals may fall below that viability threshold. The gene(s) reducing vigor for all hybrids may not be polymorphic, in which case the genes we identify with the technique used in this paper will not be DMIs, but alleles that generally lower vigor (possibly acting in the same way in hybrids as in pure species). These genes still contribute to inviability, but may not be DMIs in the true sense of AaBb heterozygotes doing poorly.