Sex ratio affects sexual selection against mutant alleles in a locus-specific way.

Higher male:female operational sex ratio (OSR) is often assumed to lead to stronger sexual selection on males. Yet, this premise has been directly tested by very few studies, with mixed outcomes. We investigated how OSR affects the strength of sexual selection against two deleterious alleles, a natural ebony mutant and a transgenic GFP insertion, in Drosophila melanogaster. To this end, we estimated the relative paternity share of homozygous mutant males competing against wild-type males under different OSRs (1:2, 1:1, 2:1). We also manipulated the mating pool density (18, 36, or 54 individuals) and assessed paternity over three consecutive days, during which the nature of sexual interaction changed. The strength of sexual selection against the ebony mutant increased with OSR, became weaker after the first day, and was little affected by density. In contrast, sexual selection against the GFP transgene was markedly affected by density: at the highest density, it increased with OSR, but at lower densities, it was strongest at 1:1 OSR, remaining strong throughout the experiment. Thus, while OSR can strongly affect the strength of sexual selection against "bad genes," it does not necessarily increase monotonically with male:female OSR. Furthermore, the pattern of relationship between OSR and the strength of sexual selection can be locus-specific, likely reflecting the specific phenotypic effects of the mutation.

Adaptation to a bacterial pathogen in Drosophila melanogaster is not aided by sexual selection.

Theory predicts that sexual selection should aid adaptation to novel environments, but empirical support for this idea is limited. Pathogens are a major driver of host evolution and, unlike abiotic selection pressures, undergo epidemiological and co-evolutionary cycles with the host involving adaptation and counteradaptation. Because of this, populations harbor ample genetic variation underlying immunity and the opportunity for sexual selection based on condition-dependent "good genes" is expected to be large. In this study, we evolved populations of Drosophila melanogaster in a 2-way factorial design manipulating sexual selection and pathogen presence, using a gram-negative insect pathogen Pseudomonas entomophila, for 14 generations. We then examined how the presence of sexual selection and the pathogen, as well as any potential interaction, affected the evolution of pathogen resistance. We found increased resistance to P. entomophila in populations that evolved under pathogen pressure, driven primarily by increased female survival after infection despite selection for resistance acting only on males over the course of experimental evolution. This result suggests that the genetic basis of resistance is in part shared between the sexes. We did not find any evidence of sexual selection aiding adaptation to pathogen, however, a finding contrary to the predictions of "good genes" theory. Our results therefore provide no support for a role for sexual selection in the evolution of immunity in this experimental system.

Predator-induced maternal effects determine adaptive antipredator behaviors via egg composition.

In high-risk environments with frequent predator encounters, efficient antipredator behavior is key to survival. Parental effects are a powerful mechanism to prepare offspring for coping with such environments, yet clear evidence for adaptive parental effects on offspring antipredator behaviors is missing. Rapid escape reflexes, or "C-start reflexes," are a key adaptation in fish and amphibians to escape predator strikes. We hypothesized that mothers living in high-risk environments might induce faster C-start reflexes in offspring by modifying egg composition. Here, we show that offspring of the cichlid fish Neolamprologus pulcher developed faster C-start reflexes and were more risk averse if their parents had been exposed to cues of their most dangerous natural predator during egg production. This effect was mediated by differences in egg composition. Eggs of predator-exposed mothers were heavier with higher net protein content, and the resulting offspring were heavier and had lower igf-1 gene expression than control offspring shortly after hatching. Thus, changes in egg composition can relay multiple putative pathways by which mothers can influence adaptive antipredator behaviors such as faster escape reflexes.

Bi-stability in type 2 diabetes mellitus multi-organ signalling network.

Type 2 diabetes mellitus (T2DM) is believed to be irreversible although no component of the pathophysiology is irreversible. We show here with a network model that the apparent irreversibility is contributed by the structure of the network of inter-organ signalling. A network model comprising all known inter-organ signals in T2DM showed bi-stability with one insulin sensitive and one insulin resistant attractor. The bi-stability was made robust by multiple positive feedback loops suggesting an evolved allostatic system rather than a homeostatic system. In the absence of the complete network, impaired insulin signalling alone failed to give a stable insulin resistant or hyperglycemic state. The model made a number of correlational predictions many of which were validated by empirical data. The current treatment practice targeting obesity, insulin resistance, beta cell function and normalization of plasma glucose failed to reverse T2DM in the model. However certain behavioural and neuro-endocrine interventions ensured a reversal. These results suggest novel prevention and treatment approaches which need to be tested empirically.