Sir2, an evolutionarily conserved NAD(+)-dependent deacetylase, has been implicated as a key factor in mediating organismal life span. However, recent contradictory findings have brought into question the role of Sir2 and its orthologs in regulating organismal longevity. In this study, we report that Drosophila Sir2 (dSir2) in the adult fat body regulates longevity in a diet-dependent manner. We used inducible Gal4 drivers to knock down and overexpress dSir2 in a tissue-specific manner. A diet-dependent life span phenotype of dSir2 perturbations (both knockdown and overexpression) in the fat body, but not muscles, negates the effects of background genetic mutations. In addition to providing clarity to the field, our study contrasts the ability of dSir2 in two metabolic tissues to affect longevity. We also show that dSir2 knockdown abrogates fat-body dFOXO-dependent life span extension. This report highlights the importance of the interplay between genetic factors and dietary inputs in determining organismal life spans.

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.

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.

When the cost of reproduction for males and variance in female quality are high, males are predicted to show adaptive mate choice. Using Drosophila melanogaster, we test this prediction and show that sperm limited males preferentially mated with young and/or well fed females. The preferred females had higher reproductive output – direct evidence of adaptive precopulatory male mate choice. Our most striking finding is the strong positive correlation between the degree of mating bias showed by the males and the variance in the fitness of the females. We discuss the possible mechanism for such adaptive male mate choice and propose that such choice has important consequences with respect to the existing understanding of the mating system and the evolution of aging.

Promiscuity can drive the evolution of sexual conflict before and after mating occurs. Post mating, the male ejaculate can selfishly manipulate female physiology, leading to a chemical arms race between the sexes. Theory suggests that drift and sexually antagonistic coevolution can cause allopatric populations to evolve different chemical interactions between the sexes, thereby leading to postmating reproductive barriers and speciation. There is, however, little empirical evidence supporting this form of speciation. We tested this theory by creating an experimental evolutionary model of Drosophila melanogaster populations undergoing different levels of interlocus sexual conflict. We found that allopatric populations under elevated sexual conflict show assortative mating, indicating premating reproductive isolation. Further, these allopatric populations also show reduced copulation duration and sperm defense ability when mating happens between individuals across populations compared to that within the same population, indicating postmating prezygotic isolation. Sexual conflict can cause reproductive isolation in allopatric populations through the coevolution of chemical (postmating prezygotic) as well as behavioural (premating) interactions between the sexes. Thus, to our knowledge, we provide the first comprehensive evidence of postmating (as well as premating) reproductive isolation due to sexual conflict.

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.

Sperm competition theory predicts that with increase in sperm competition, males either invest more in reproductive organ(s) and/or improve ejaculate investment. We test this idea using experimental evolution in Drosophila melanogaster. We maintained replicate populations of Drosophila melanogaster under male (M) and female (F) biased sex ratio regimes for more than a hundred generations with the result that males from the M regime evolved higher sperm competitive abilities relative to males from the F regime. In the present study, we measured the testes and the accessory gland size of virgin and singly mated males from the M and F regimes. The M and F males do not differ in either testis or accessory gland size. Additionally, ejaculate investment is not different in the M and F males, as measured by reduction in testis and accessory gland sizes. Thus, contrary to theoretical prediction and evidence from other species, we found that evolved differences in sperm competitive ability are not necessarily due to evolution of testis/accessory gland size or strategic ejaculate investment in these populations.