Does Sex Trade with Violence among Genotypes in Drosophila melanogaster?

The evolutionary forces shaping the ability to win competitive interactions, such as aggressive encounters, are still poorly understood. Given a fitness advantage for competitive success, variance in aggressive and sexual display traits should be depleted, but a great deal of variation in these traits is consistently found. While life history tradeoffs have been commonly cited as a mechanism for the maintenance of variation, the variability of competing strategies of conspecifics may mean there is no single optimum strategy. We measured the genetically determined outcomes of aggressive interactions, and the resulting effects on mating success, in a panel of diverse inbred lines representing both natural variation and artificially selected genotypes. Males of one genotype which consistently lost territorial encounters with other genotypes were nonetheless successful against males that were artificially selected for supernormal aggression and dominated all other lines. Intransitive patterns of territorial success could maintain variation in aggressive strategies if there is a preference for territorial males. Territorial success was not always associated with male mating success however and females preferred ‘winners’ among some male genotypes, and ‘losers’ among other male genotypes. This suggests that studying behaviour from the perspective of population means may provide limited evolutionary and genetic insight. Overall patterns of competitive success among males and mating transactions between the sexes are consistent with mechanisms proposed for the maintenance of genetic variation due to nonlinear outcomes of competitive interactions

Atrial fibrillation genetic risk differentiates cardioembolic stroke from other stroke subtypes

AbstractObjectiveWe sought to assess whether genetic risk factors for atrial fibrillation can explain cardioembolic stroke risk.MethodsWe evaluated genetic correlations between a prior genetic study of AF and AF in the presence of cardioembolic stroke using genome-wide genotypes from the Stroke Genetics Network (N = 3,190 AF cases, 3,000 cardioembolic stroke cases, and 28,026 referents). We tested whether a previously-validated AF polygenic risk score (PRS) associated with cardioembolic and other stroke subtypes after accounting for AF clinical risk factors.ResultsWe observed strong correlation between previously reported genetic risk for AF, AF in the presence of stroke, and cardioembolic stroke (Pearson’s r=0.77 and 0.76, respectively, across SNPs with p &lt; 4.4 × 10−4 in the prior AF meta-analysis). An AF PRS, adjusted for clinical AF risk factors, was associated with cardioembolic stroke (odds ratio (OR) per standard deviation (sd) = 1.40, p = 1.45×10−48), explaining ∼20% of the heritable component of cardioembolic stroke risk. The AF PRS was also associated with stroke of undetermined cause (OR per sd = 1.07, p = 0.004), but no other primary stroke subtypes (all p &gt; 0.1).ConclusionsGenetic risk for AF is associated with cardioembolic stroke, independent of clinical risk factors. Studies are warranted to determine whether AF genetic risk can serve as a biomarker for strokes caused by AF.</jats:sec

Data from: Does phenotypic plasticity for adult size versus food level in Drosophila melanogaster evolve in response to adaptation to different rearing densities?

Recent studies using inbred lines of Drosophila have suggested that there is extensive genetic variability for phenotypic plasticity of body size versus food level. If true, we expect that the outcome of evolution at very different food levels should yield genotypes whose adult sizes show different patterns of phenotypic plasticity. We have tested this prediction with six independent populations of Drosophila melanogaster kept at extreme (low vs. high) densities for 125 generations. We found that the phenotypic plasticity of body size versus food level is not affected by selection or the presence of competitors of a different genotype. However, we document increasing among population variation in phenotypic plasticity due to random genetic drift. Several reasons are explored to explain these results including the possibility that the use of highly inbred lines to make inferences about the evolution of genetically variable populations may be misleading

female thorax size

Each line in this file correspond to the thorax size for one female. In addition to her size there is information about the (i)block, (ii) population, (iii) selection regime, and (iv) yeast level

Net reproductive rate per female.

<p>This measure includes all adults that were available for collection each generation during the normal collection period. Populations entered the thermal stress regime in generation 6. There was no difference between treatments (p = 0.63). Error bars are ± one standard error. See <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0111148#pone-0111148-t001" target="_blank">Table 1a</a>.</p

Total surviving adult progeny per female.

<p>Populations entered the thermal stress regime in generation 6. There was no difference between treatments (p = 0.64). Error bars are ± one standard error. See <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0111148#pone-0111148-t001" target="_blank">Table 1b</a>.</p

Analysis of covariance of treatment and time with respect to net reproductive rate, total surviving adult progeny, and female survival.

<p>Analysis of covariance of treatment and time with respect to net reproductive rate, total surviving adult progeny, and female survival.</p