Evolutionary consequences of sex-specific selection

Sex-specific selection is widespread, evident by the evolution of sexual dimorphism in many traits in sexually reproducing taxa. The reason why the sexes may experience selection that differs in direction or magnitude is often linked to the reproductive strategies associated with the sex-specific reproductive physiology. Competition for mates or fertilisations creates conditions where selection is sex-specific and may overall be stronger on the sex experiencing more competition. However, the sexes share a majority of their genome and consequently many traits may be genetically correlated between the sexes, constraining sex-specific adaptation. In paper I, II and III, I investigate the consequences of exposure to altered strength of sex-specific selection in the laboratory through 30 generations of experimental evolution with skewed sex ratios, using the sexually reproducing nematode Caenorhabditis remanei as a model organism. I created female-biased (FB) and male-biased (MB) treatments. In paper I, I investigated the phenotypic response to selection in three life history traits (body size, fitness and heat shock resistance as a proxy for somatic maintenance). I found a sex-specific response to the evolutionary treatments for body size and fitness, while somatic maintenance was similarly affected by the treatments in the sexes. Subsequently, in paper II, I examined sex-specific patterns of additive genetic variance (VA) for reproductive fitness, and estimated the intersexual genetic correlation (rmf) of fitness. Results show low levels of VA for fitness, and no changes in response to treatments. Values of rmf are associated with large uncertainties, highlighting the difficulties in estimating and interpreting rmf for fitness. In paper III, I used a multivariate approach to investigate the sex-specific genetic variance-covariance matrices (GF and GM), and the between-sex genetic covariance matrix (B) in the three life history traits. Results show no genetic covariances between the traits, and no covariances between the sexes in these traits. The sex-specific G-matrices also remained stable in response to the treatments. These results therefore suggest that the genetic architecture of the traits studied here does not constrain the independent evolution in the sexes. In paper IV, using the seed beetle Callosobruchus maculatus as the model, I find that experimentally induced mutations have stronger negative effects on male than female fitness, suggesting overall stronger selection on males. The results support the theory that strong sexual selection on males have the potential to purge deleterious mutations from a population.