A sexually selected male weapon characterized by strong additive genetic variance and no evidence for sexually antagonistic polyphenic maintenance.

Sexual selection and sexual antagonism are important drivers of eco-evolutionary processes. The evolution of traits shaped by these processes depends on their genetic architecture, which remains poorly studied. Here, implementing a quantitative genetics approach using diallel crosses of the bulb mite, Rhizoglyphus robini, we investigated the genetic variance that underlies a sexually selected weapon that is dimorphic among males and female fecundity.

Selection in males purges the mutation load on female fitness.

Theory predicts that the ability of selection and recombination to purge mutation load is enhanced if selection against deleterious genetic variants operates more strongly in males than females. However, direct empirical support for this tenet is limited, in part because traditional quantitative genetic approaches allow dominance and intermediate-frequency polymorphisms to obscure the effects of the many rare and partially recessive deleterious alleles that make up the main part of a population's mutation load. Here, we exposed the partially recessive genetic load of a population of seed beetles via successive generations of inbreeding, and quantified its effects by measuring heterosis-the increase in fitness experienced when masking the effects of deleterious alleles by heterozygosity-in a fully factorial sex-specific diallel cross among 16 inbred strains.

Social history and exposure to pathogen signals modulate social status effects on gene regulation in rhesus macaques.

Social experience is an important predictor of disease susceptibility and survival in humans and other social mammals. Chronic social stress is thought to generate a proinflammatory state characterized by elevated antibacterial defenses and reduced investment in antiviral defense. Here we manipulated long-term social status in female rhesus macaques to show that social subordination alters the gene expression response to ex vivo bacterial and viral challenge.

Signatures of divergent anti-malarial treatment responses in peripheral blood from adults and young children in Malawi.

Background: Heterogeneity in the immune response to parasite infection is mediated in part by differences in host genetics, gender, and age group. In infants and young children, ongoing immunological maturation often results in increased susceptibility to infection and variable responses to drug treatment, increasing the risk of complications. Even though significant age-associated effects on host cytokine responses to Plasmodium falciparum infection have been identified, age-associated effects on uncomplicated malaria infection and anti-malarial treatment remain poorly understood.