Recent data indicate that selective sweeps affect the diversity levels only at very limited distances from the selected site [e.g. [ 59, 60]], and it might be unlikely to expect selective sweeps to occur frequently enough to reduce diversity levels over the entire chromosome.
Therefore, one might expect stronger selection by pathogen-driven selective forces (heterozygote advantage, frequency dependent selection and fluctuating selection [26]) in our population than in populations with a lower pathogen load.
One might expect that the cumulative selective effect of mismatched binding preferences at hundreds of loci would outweigh any adaptive gains from transcription factor modification, yet the observed SP1 cis-regulatory modifications contradict this assumption.
Accordingly, one might expect to see a selective advantage in shutting down neo-Y linked geneo-Y linked dosagenesmpensathaton the neo-X are thus expressedosageoo high levels in males.
As one might expect, students starting at more selective institutions were less likely to keep HOPE for four years than comparable students starting at less selective institutions.
Given that synonymous sites can be subject to selection for specific tRNA anticodons, one might expect them to be under more selective constraints than intergenic regions; therefore, it is not surprising that nucleotide diversity for the intergenic regions is greater than πsyn.
Even though we might expect HBD to be subject to much lower selective pressure than HBB, in a previous study analyzing a small number of African individuals HBD was found to have lower diversity levels than HBB Websterr et al. 2003).
Based on the yeast results discussed here, one might expect that targeting mTORC2 will trigger a more selective and synergistic cell death, than pan-mTOR or pan-PIKK inhibitors.
If a lower heritability or a smaller population size were used, one might expect to see a greater benefit from using the selective method.
