BackgroundInterlocus conflict predicts (a) evolution of traits, beneficial to males but detrimental to females and (b) evolution of aging and life-span under the influence of the cost of bearing these traits. However, there are very few empirical investigations shedding light on these predictions. Those that do address these issues, mostly reported response of male reproductive traits or the lack of it and do not address the life-history consequence of such evolution. Here, we test both the above mentioned predictions using experimental evolution on replicate populations of Drosophila melanogaster. We present responses observed after >45 generations of altered levels of interlocus conflict (generated by varying the operational sex ratio).ResultsMales from the male biased (high conflict, M-regime) regime evolved higher spontaneous locomotor activity and courtship frequency. Females exposed to these males were found to have higher mortality rate. Males from the female biased regime (low conflict, F-regime) did not evolve altered courtship frequency and activity. However, progeny production of females continuously exposed to F-males was significantly higher than the progeny production of females exposed to M-males indicating that the F-males are relatively benign towards their mates. We found that males from male biased regime lived shorter compared to males from the female biased regime.ConclusionF-males (evolving under lower levels of sexual conflict) evolved decreased mate harming ability indicating the cost of maintenance of the suit of traits that cause mate-harm. The M-males (evolving under higher levels sexual conflict) caused higher female mortality indicating that they had evolved increased mate harming ability, possibly as a by product of increased reproduction related activity. There was a correlated evolution of life-history of the M and F-males. M-regime males lived shorter compared to the males from F-regime, possibly due to the cost of investing more in reproductive traits. In combination, these results suggest that male reproductive traits and life-history traits can evolve in response to the altered levels of interlocus sexual conflict.

In naturally polygamous organisms such as Drosophila, sperm competitive ability is one of the most important components of male fitness and is expected to evolve in response to varying degrees of male-male competition. Several studies have documented the existence of ample genetic variation in sperm competitive ability of males. However, many experimental evolution studies have found sperm competitive ability to be unresponsive to selection. Even direct selection for increased sperm competitive ability has failed to yield any measurable changes. Here we report the evolution of sperm competitive ability (sperm defense-P1, offense-P2) in a set of replicate populations of Drosophila melanogaster subjected to altered levels of male-male competition (generated by varying the operational sex ratio) for 55-60 generations. Males from populations with female-biased operational sex ratio evolved reduced P1 and P2, without any measurable change in the male reproductive behavior. Males in the male-biased regime evolved increased P1, but there was no significant change in P2. Increase in P1 was associated with an increase in copulation duration, possibly indicating greater ejaculate investment by these males. This study is one of the few to provide empirical evidence for the evolution of sperm competitive ability of males under different levels of male-male competition.

Viruses are major evolutionary drivers of insect immune systems. Much of our knowledge of insect immune responses derives from experimental infections using the fruit fly Drosophila melanogaster. Most experiments, however, employ lethal pathogen doses through septic injury, frequently overwhelming host physiology. While this approach has revealed several immune mechanisms, it is less informative about the fitness costs hosts may experience during infection in the wild. Using both systemic and oral infection routes, we find that even apparently benign, sublethal infections with the horizontally transmitted Drosophila C virus (DCV) can cause significant physiological and behavioural morbidity that is relevant for host fitness. We describe DCV-induced effects on fly reproductive output, digestive health and locomotor activity, and we find that viral morbidity varies according to the concentration of pathogen inoculum, host genetic background and sex. Notably, sublethal DCV infection resulted in a significant increase in fly reproduction, but this effect depended on host genotype. We discuss the relevance of sublethal morbidity for Drosophila ecology and evolution, and more broadly, we remark on the implications of deleterious and beneficial infections for the evolution of insect immunity.

BackgroundMaintenance and deployment cost of immunity is high, therefore, it is expected to trade-off with other high cost traits like sexual activity. Previous studies with Drosophila melanogaster show that male’s ability to clear bacteria decreases with increase in sexual activity. We subjected this idea to test using two pathogens (Pseudomonas entomophila and Staphylococcus succinus) and three different populations of Drosophila melanogaster.ResultsWe found that sexual activity enhanced male survivorship in a pathogen specific manner. Sexually active males show higher resistance than virgins upon infection with Pseudomonas entomophila. Interestingly, the beneficial effects of sexual activity increased with time of co-habitation with females and declined when access to females was restricted. We observed no change in male survivorship upon experimentally varying the number of sexual interactions.ConclusionOur results show that the sexual activity-immunity trade-off in males cannot be generalised. The trade-off is potentially mediated through complex interactions between the host, pathogen and the environment experienced by the host.

Maintenance and deployment of the immune system are costly and are hence predicted to trade-off with other resource-demanding traits, such as reproduction. We subjected this longstanding idea to test using laboratory experimental evolution approach. In the present study, replicate populations of Drosophila melanogaster were subjected to three selection regimes-I (Infection with Pseudomonas entomophila), S (Sham-infection with MgSO4 ), and U (Unhandled Control). After 30 generations of selection flies from the I regime had evolved better survivorship upon infection with P. entomophila compared to flies from U and S regimes. However, contrary to expectations and previous reports, we did not find any evidence of trade-offs between immunity and other life history related traits, such as longevity, fecundity, egg hatchability, or development time. After 45 generations of selection, the selection was relaxed for a set of populations. Even after 15 generations, the postinfection survivorship of populations under relaxed selection regime did not decline. We speculate that either there is a negligible cost to the evolved immune response or that trade-offs occur on traits such as reproductive behavior or other immune mechanisms that we have not investigated in this study. Our research suggests that at least under certain conditions, life-history trade-offs might play little role in maintaining variation in immunity.

The ability to tolerate infection is a key component of host defence and offers potential novel therapeutic approaches for infectious diseases. To yield successful targets for therapeutic intervention, it is important that the analytical tools employed to measure disease tolerance are able to capture distinct host responses to infection. Here, we show that commonly used methods that estimate tolerance as a linear relationship should be complemented with more flexible, nonlinear estimates of this relationship which may reveal variation in distinct components such as host vigour, sensitivity to increases in pathogen loads, and the severity of the infection. To illustrate this, we measured the survival of Drosophila melanogaster carrying either a functional or non-functional regulator of the JAK-STAT immune pathway (G9a) when challenged with a range of concentrations of Drosophila C virus (DCV). While classical linear model analyses indicated that G9a affected tolerance only in females, a more powerful nonlinear logistic model showed that G9a mediates viral tolerance to different extents in both sexes. This analysis also revealed that G9a acts by changing the sensitivity to increasing pathogen burdens, but does not reduce the ultimate severity of disease. These results indicate that fitting nonlinear models to host health–pathogen burden relationships may offer better and more detailed estimates of disease tolerance.

Bacterial symbionts are widespread among metazoans and provide a range of beneficial functions. Wolbachia-mediated protection against viral infection has been extensively demonstrated in Drosophila. In mosquitoes that are artificially transinfected with Drosophila melanogaster Wolbachia (wMel), protection from both viral and bacterial infections has been demonstrated. However, no evidence for Wolbachia-mediated antibacterial protection has been demonstrated in Drosophila to date. Here, we show that the route of infection is key for Wolbachia-mediated antibacterial protection. Drosophila melanogaster carrying Wolbachia showed reduced mortality during enteric—but not systemic—infection with the opportunist pathogen Pseudomonas aeruginosa. Wolbachia-mediated protection was more pronounced in male flies and is associated with increased early expression of the antimicrobial peptide Attacin A, and also increased expression of a reactive oxygen species detoxification gene (Gst D8). These results highlight that the route of infection is important for symbiont-mediated protection from infection, that Wolbachia can protect hosts by eliciting a combination of resistance and disease tolerance mechanisms, and that these effects are sexually dimorphic. We discuss the importance of using ecologically relevant routes of infection to gain a better understanding of symbiont-mediated protection.

Males and females are subjected to distinct kinds of selection pressures, often leading to the evolution of sex‐specific genetic architecture, an example being sex‐specific dominance. Sex‐specific dominance reversals (SSDRs), where alleles at sexually antagonistic loci are at least partially dominant in the sex they benefit, have been documented in Atlantic salmon, rainbow trout, and seed beetles. Another interesting feature of many sexually reproducing organisms is the asymmetric inheritance pattern of X chromosomes, which often leads to distinct evolutionary outcomes on X chromosomes compared to autosomes. Examples include the higher efficacy of sexually concordant selection on X chromosomes, and X chromosomes being more conducive to the maintenance of sexually antagonistic polymorphisms under certain conditions. Immunocompetence is a trait that has been extensively investigated for sexual dimorphism with growing evidence for sex‐specific or sexually antagonistic variation. X chromosomes have been shown to harbor substantial immunity‐related genetic variation in the fruit fly, Drosophila melanogaster. Here, using interpopulation crosses and cytogenetic cloning, we investigated sex‐specific dominance and the role of the X chromosome in improved postinfection survivorship of laboratory populations of D. melanogaster selected against pathogenic challenge by Pseudomonas entomophila. We could not detect any contribution of the X chromosome to the evolved immunocompetence of our selected populations, as well as to within‐population variation in immunocompetence. However, we found strong evidence of sex‐specific dominance related to surviving bacterial infection. Our results indicate that alleles that confer a survival advantage to the selected populations are, on average, partially dominant in females but partially recessive in males. This could also imply an SSDR for overall fitness, given the putative evidence for sexually antagonistic selection affecting immunocompetence in Drosophila melanogaster. We also highlight sex‐specific dominance as a potential mechanism of sex differences in immunocompetence, with population‐level sex differences primarily driven by sex differences in heterozygotes.