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Unlike mammals, zebrafish possess a remarkable ability to regenerate damaged retina after an acute injury. Retina regeneration in zebrafish involves the induction of Müller glia-derived progenitor cells (MGPCs) exhibiting stem cell-like characteristics, which are capable of restoring all retinal cell-types. The induction of MGPC through Müller glia-reprograming involves several cellular, genetic and biochemical events soon after a retinal injury. Despite the knowledge on the importance of Phosphatase and tensin homolog (Pten), which is a dual-specificity phosphatase and tumor suppressor in the maintaining of cellular homeostasis, its importance during retina regeneration remains unknown. Here, we explored the importance of Pten during zebrafish retina regeneration. The Pten gets downregulated upon retinal injury and is absent from the MGPCs, which is essential to trigger Akt-mediated cellular proliferation essential for retina regeneration. We found that the downregulation of Pten in the post-injury retina accelerates MGPCs formation, while its overexpression restricts the regenerative response. We observed that Pten regulates the proliferation of MGPCs not only through Akt pathway but also by Mmp9/Notch signaling. Mmp9-activity is essential to induce the proliferation of MGPCs in the absence of Pten. Lastly, we show that expression of Pten is fine-tuned through Mycb/histone deacetylase1 and Tgf-β signaling. The present study emphasizes on the stringent regulation of Pten and its crucial involvement during the zebrafish retina regeneration.

Male-biased operational sex ratios can increase male-male competition and can potentially select for both increased pre- and postcopulatory male success. In the present study, using populations of Drosophila melanogaster evolved under male-biased (M) or female-biased (F) sex ratios, we asked whether (a) male mating success can evolve, (b) males are better at mating females that they have coevolved with, (c) males mating success is affected by female mating status, and (d) male mating success is correlated with their courtship effort. We directly competed M and F males for mating with (a) virgin ancestral (common) females, (b) virgin females from the M and F populations, and (c) singly mated females from the M and F populations. We also assessed the courtship frequency of the males when paired with mated M or F females. Our results show that M males, evolving under an increased level of male-male competition, have higher mating success than F males irrespective of the female evolutionary history. However, the difference in mating success is more pronounced if the females had mated before. M males also have a higher courtship frequency than F males, but we did not find any correlation between mating success and courtship frequency.

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.

Sexual activity (mating) negatively affects immune function in various insect species, in both sexes. In the experiments reported in this manuscript, we tested if hosts adapted to regular pathogen challenges are less susceptible to mating induced immune suppression, using experimentally evolved Drosophila melanogaster populations selected for increased post-infection survival when infected with a Gram-positive bacterium, Enterococcus faecalis. Mating increased susceptibility of females to bacterial pathogens, but in a pathogen specific manner. Mating-induced increase in susceptibility was also affected by host evolutionary history, with females from selected populations exhibiting similar post-infection survival irrespective of mating status, while females from control populations became more susceptible to bacterial infections after mating. Post-infection survival of males, irrespective of their evolutionary history, was not affected by their mating status. We therefore conclude that hosts evolved to better survive bacterial infections are also better at resisting mating-induced increase in susceptibility to infections in Drosophila melanogaster.

Evolution of increased immune defence is often limited by costs: correlated changes in other traits (viz. life-history traits) that otherwise reduce the fitness of the host organisms. Experimental evolution studies are useful for understanding the evolution of immune function, and correlated changes in other traits. We experimentally evolved replicate Drosophila melanogaster populations to better survive infection challenge with an entomopathogenic bacteria, Enterococcus faecalis. Within 35 generations of forward selection, selected populations showed marked increase in post-infection survival compared to ancestrally paired controls. We next measured various life-history traits of these populations. Our results show that the selected populations do not differ from control populations for larval development time and body weight at eclosion. No difference is also observed in case of fecundity and longevity (following the acute phase of infection), either when the flies are subjected to infection or when the flies were uninfected; although infected flies from all populations die much earlier compared to uninfected flies. Selected flies and control flies are also equally good at surviving abiotic stressors (starvation and desiccation), although infected flies from all populations are more susceptible to stress than uninfected flies. Therefore, we conclude that (a) D. melanogaster populations can rapidly evolve to be more immune to infection with E. faecalis; (b) evolution of increased defence against E. faecalis entails no life-history cost for the hosts; and (c) evolving defence against a biotic threat (pathogen) does not make flies more resistant to abiotic stressors.

In the experiments reported in this manuscript, we explore the effect of bacterial infections on the reproductive output of Drosophila melanogaster females. Canonical view of host-pathogen interactions supposes two possible outcomes. Because of immune defence being an energy/resource intensive function, an infected female reallocates resources away from reproductive processes and towards immune defence, therefore compromising its reproductive output. Alternatively, faced with impending mortality, an infected female increases its reproductive output to compensate for lost opportunities of future reproduction. We tested if pathogen identity, infection outcome (survival vs. death), and/or time of death determines the reproductive output of females infected with three bacterial pathogens. Our results show that pathogen identity is a reliable predictor of population level response of infected females but does not reliably predict the behaviour of individual females. Additionally, females succumbing to infection exhibit greater variability in reproductive output, compared to both survivors and controls, but this variability is not explained by either the time of death or the identity of the infecting pathogen. Furthermore, survivors of infection have reproductive output similar to control females.

Rapid exaggeration of host and pathogen traits via arms race dynamics is one possible outcome of host–pathogen coevolution. However, the exaggerated traits are expected to incur costs in terms of resource investment in other life-history traits. The current study investigated the costs associated with evolved traits in a host–pathogen coevolution system. We used the Drosophila melanogaster (host) –Pseudomonas entomophila (pathogen) system to experimentally derive two selection regimes, one where the host and pathogen both coevolved, and the other, where only the host evolved against a non-evolving pathogen. After 17 generations of selection, we found that hosts from both selected populations had better post-infection survivorship than controls. Even though the coevolving populations tended to have better survivorship post-infection, we found no clear evidence that the two selection regimes were significantly different from each other. There was weak evidence for the coevolving pathogens being more virulent than the ancestral pathogen. We found no major cost of increased post-infection survivorship. The costs were not different between the coevolving hosts and the hosts evolving against a non-evolving pathogen. We found no evolved costs in the coevolving pathogens. Thus, our results suggest that increased host immunity and pathogen virulence may not be costly.

In the experiments presented here, we explore the effect of resource limitation, in form of starvation (which leads to decrease in accessible resources and depletion of reserves) and sexual activity (which leads to reallocation of resources from somatic defence towards reproduction), on immune function of female Drosophila melanogaster flies. We infected females with five bacterial pathogens and measured their post-infection survival when subjected to either starvation or sexual activity (mating). Additionally, we measured within host pathogen levels in case of three of these pathogens. Based on previous literature, we predicted that both modes of resource limitation will increase post-infection mortality, but only sexual activity will lead to increase of pathogen load (because of compromised immune function), while starvation will either not affect or reduce pathogen loads (because of reduced availability of resources for the pathogen to proliferate within the host). Our results indicate that both starvation and sexual activity can lead to increased within-host pathogen levels, in addition to increased post-infection mortality, but in a pathogen-specific manner.

The ability to thermal adaptation can alter insects’ reproductive traits and physiologic response. A number of studies in Drosophila documented the higher expression levels of heat shock proteins (Hsps) and Frost (Fst) genes during the recovery phase of cold shock treatment and suggested that higher expression levels of these genes and lipids can protect from cold stress. However, these genes’ expression and cold adaptation have not been well studied. Therefore, understanding the molecular and biochemical basis of cold adaptation, we examined the levels of lipid and expression patterns of Hsp22, Hsp23, Hsp40, Hsp68, Hsp70, Hsp 83, and Fst genes under the cold stress or benign condition in the populations of Drosophila melanogaster selected for increased resistance to cold shock.We observed the significant up-regulation of Hsp22, Hsp23, Hsp40, Hsp68, and Fst genes in the FSB and FCB populations during the recovery phase post cold shock compared to the no shock condition. However, there was not a significant change in the transcript levels of these genes between FSB and FCB under both the cold stress or no shock condition. Additionally, we noticed higher total lipid levels in the females from cold shock treatment than those from no shock treatment. This finding suggests that cold selected populations have different mechanisms to sustain cold stress.

Mounting an immune response requires a considerable energy investment by the host. This makes expression of immune phenotypes susceptible to changes in availability of resources. There is ample evidence in scientific literature to suggest that hosts become more vulnerable to infection by pathogens and parasites when access to nutrition is limited. Using populations of Drosophila melanogaster experimentally evolved to better survive bacterial infections, we explore if host selection history influences host response to resource deprivation in terms of immune function. We find that when reared on a suboptimal diet (both in larval and adult stages), adult flies from evolved populations are still more immune to infections compared to flies from control populations. Furthermore, we observe a sex-dependent effect of interaction between selection history and diet on immune function. We thus conclude that immune function of hosts adapted to pathogen challenge is less affected by resource limitation compared to non-adapted hosts.

The density-dependent prophylaxis hypothesis predicts that risk of pathogen transmission increases with increase in population density, and in response to this, organisms mount a prophylactic immune response when exposed to high density. This prophylactic response is expected to help organisms improve their chances of survival when exposed to pathogens. Alternatively, organisms living at high densities can exhibit compromised defense against pathogens due to lack of resources and density associated physiological stress; the density stress hypothesis. We housed adult Drosophila melanogaster flies at different densities and measured the effect this has on their post-infection survival and resistance to starvation. We find that flies housed at higher densities show greater mortality after being infected with bacterial pathogens, while also exhibiting increased resistance to starvation. Our results are more in line with the density-stress hypothesis that postulates a compromised immune system when hosts are subjected to high densities.

The host susceptibility to one pathogen can decrease, increase, or remain unaffected by virtue of the host evolving resistance towards a second pathogen. Negative correlations between a host susceptibility to different pathogens is an often-cited explanation for maintenance of genetic variation in immune function determining traits in a host population. In this study, we investigated the change in susceptibility of Drosophila melanogaster flies to various novel bacterial pathogens after being experimentally selected for increased resistance to one particular bacterial pathogen. We independently selected flies to become more resistant towards Enterococcus faecalis and Pseudomonas entomophila, and baring a few exceptions the evolved populations exhibited cross-resistance against the range of pathogens tested in the study. Neither the identity of the native pathogen nor the host sex was major determining factors in predicting the pattern of cross-resistance exhibited by the selected populations. We therefore report that a generalized cross-resistance to novel pathogens can repeatedly evolve in response to selection for resistance against a single pathogen.

Background Divergence in the evolutionary interests of males and females leads to sexual conflict. Traditionally, sexual conflict has been classified into two types: inter-locus sexual conflict (IeSC) and intra-locus sexual conflict (IaSC). IeSC is modeled as a conflict over outcomes of intersexual reproductive interactions mediated by loci that are sex-limited in their effects. IaSC is thought to be a product of selection acting in opposite directions in males and females on traits with a common underlying genetic basis. While in their canonical formalisms IaSC and IeSC are mutually exclusive, there is growing support for the idea that the two may interact. Empirical evidence for such interactions, however, is limited. Results Here, we investigated the interaction between IeSC and IaSC in Drosophila melanogaster. Using hemiclonal analysis, we sampled 39 hemigenomes from a laboratory-adapted population of D. melanogaster. We measured the contribution of each hemigenome to adult male and female fitness at three different intensities of IeSC, obtained by varying the operational sex ratio. Subsequently, we estimated the intensity of IaSC at each sex ratio by calculating the intersexual genetic correlation (rw,g,mf) for fitness and the proportion of sexually antagonistic fitness-variation. We found that the intersexual genetic correlation for fitness was positive at all three sex ratios. Additionally, at male biased and equal sex ratios the rw,g,mf was higher, and the proportion of sexually antagonistic fitness variation lower, relative to the female biased sex ratio, although this trend was not statistically significant. Conclusion Our results indicate a statistically non-significant trend suggesting that increasing the strength of IeSC ameliorates IaSC in the population.

The ability to tolerate temperature stress is an important component of adult fitness. In holometabolous insects like Drosophila melanogaster, adult stress resistance can be affected by growth conditions experienced during the larval stages. Although evolution under crowded larval conditions is known to lead to the correlated evolution of many adult traits, its consequences on adult heat stress tolerance have not been investigated. Therefore, in the present study, we assessed the adult heat stress tolerance in populations of D. melanogaster adapted to a stressful larval crowding environment. We used replicate populations of D. melanogaster, selected for adaptation to larval crowding stress (MCUs), for more than 230 generations, and their respective controls (MBs). Larvae from selected and control populations were grown under crowded and uncrowded conditions, and their adult heat shock resistance at two different temperatures was measured. Further, we compared Hsp70 expression in crowded and uncrowded larvae of both populations and also measured the Hsp70 expression after a mild heat treatment in adults of selected and control populations. Our results showed that adaptation to larval crowding leads to the evolution of Hsp70 gene expression in larval stages and improves adult heat stress tolerance ability in males, but not in females.

In a multicentric, observational, investigator-blinded, and longitudinal clinical study of 764 ART-naïve subjects, we identified nine different promoter-variant strains of HIV-1 subtype C (HIV-1C) emerging in the Indian population, with some of these variants being reported for the first time. Unlike several previous studies, our work here focuses on the evolving viral regulatory elements, not coding sequences. The emerging viral strains contain additional copies of the existing transcription factor binding sites (TFBS), including TCF-1α/LEF-1, RBEIII, AP-1, and NF-κB, created by sequence duplication. The additional TFBS are genetically diverse and may blur the distinction between the modulatory region of the promoter and the viral enhancer. In a follow-up analysis, we found trends, but not significant associations between any specific variant promoter and prognostic markers, probably because the emerging viral strains might not have established mono infections yet. Illumina sequencing of four clinical samples containing a co-infection indicated the domination of one strain over the other and establishing a stable ratio with the second strain at the follow-up time-points. Since a single promoter regulates viral gene expression and constitutes the master regulatory circuit with Tat, the acquisition of additional and variant copies of the TFBS may significantly impact viral latency and latent reservoir characteristics. Further studies are urgently warranted to understand how the diverse TFBS profiles of the viral promoter may modulate the characteristics of the latent reservoir, especially following the initiation of antiretroviral therapy.

The density-dependent prophylaxis hypothesis predicts that risk of pathogen transmission increases with increase in population density, and in response to this, organisms mount a prophylactic immune response when exposed to high density. This prophylactic response is expected to help organisms improve their chances of survival when exposed to pathogens. Alternatively, organisms living at high densities can exhibit compromised defense against pathogens due to lack of resources and density associated physiological stress; the crowding stress hypothesis. We housed adult Drosophila melanogaster flies at different densities and measured the effect this has on their post-infection survival and resistance to starvation. We find that flies housed at higher densities show greater mortality after being infected with bacterial pathogens, while also exhibiting increased resistance to starvation. Our results are more in line with the crowding stress hypothesis that postulates a compromised immune system when hosts are subjected to high densities.

In many insects, the larval environment is confined to the egg-laying site, which often leads to crowded larval conditions, exposing the developing larvae to poor resource availability and toxic metabolic wastes. Larval crowding imposes two opposing selection pressures. On one hand, due to poor nutritional resources during developmental stages, adults from the crowded larval environment have reduced investment in reproductive tissues. On the other hand, a crowded larval environment acts as a cue for future reproductive competition inducing increased investment in reproductive tissues. Both these selection pressures are likely affected by the level of crowding. The evolutionary consequence of adaptation to larval crowding environment on adult reproductive investment is bound to be a result of the interaction of these two opposing forces. In this study, we used experimentally evolved populations of

Post-copulatory sexual selection (PSS) is an important selective force that determines fitness in polyandrous species. PSS can be intense in some cases and can drive the evolution of remarkable ejaculate properties. In males, investment in ejaculate plays an important role in the outcome of PSS. Thus, males are expected to adaptively tailor their ejaculate according to the perceived competition in their vicinity. Plastic responses in ejaculate investment to variation in intrasexual competition are disparate and widespread in males. We investigated the evolution of plasticity in reproductive traits using Drosophila melanogaster populations evolving for more than 150 generations under male- or female-biased sex ratios. When exposed to different numbers of competitors early in their life, males from these two regimes responded differently in terms of their copulation duration and sperm competitive ability. In addition, the effect of this early life experience wore off at different rates in males of male-biased and female-biased regimes with increasing time from the removal of competitive cues. Furthermore, our study finds that males change their reproductive strategies depending upon the identity of rival males. Together, our results provide evidence of the evolution of male reproductive investment that depends on socio-sexual cues experienced early in life.

Intralocus Sexual Conflict (IaSC) ensues when males and females of the same species experience divergent selection on shared traits. A large number of traits have been implicated in IaSC and there is growing evidence for sexual antagonism associated with immunity. X chromosomes are thought to be hotspots of sexually antagonistic genetic variation and have been shown to harbour substantial immunity-related genetic variation.Here, using interpopulation crosses and cytogenetic cloning, we investigated the role of the X chromosome in improved immune response of laboratory populations of the fruit-flyDrosophila melanogasterselected against systemic infection byPseudomonas entomophila.We could not detect any contribution of the X chromosome in the evolved immune response of our selected populations. However, we found strong evidence of sex-specific dominance related to immunity in our populations. Our results indicate that alleles that confer a superior immune response to the selected populations are, on average, partially dominant in females but partially recessive in males.We argue that sex-specific dominance over immunity evolved as a by-product of sexually antagonistic selection in the wild ancestors of our populations. We also highlight sex-specific dominance as a potential mechanism of sex differences in immunity, with population-level sex differences primarily driven by sex differences in heterozygotes.

Cold stress is a critical environmental challenge that affects an organism’s fitness-related traits. InDrosophila, increased resistance to specific environmental stress may lead to increased resistance to other kinds of stress. In the present study, we aimed to understand whether increased cold stress resistance inDrosophila melanogastercan facilitate their ability to tolerate other environmental stresses. For the current study, we used successfully selected replicate populations ofD. melanogasteragainst cold shock and their control population. These selected populations have evolved several reproductive traits, including increased egg viability, mating frequency, male mating ability, ability to sire progenies, and faster recovery for mating latency under cold shock conditions. In the present work, we investigated egg viability and mating frequency with and without heat and cold shock conditions in the selected and their control populations. We also examined resistance to cold shock, heat shock, desiccation, starvation, and survival post-challenge withStaphylococcus succinussubsp.succinusPK-1 in the selected and their control populations.After cold-shock treatment, we found a 1.25 times increase in egg viability and a 1.57 times increase in mating frequency in the selected populations compared to control populations. Moreover, more males (0.87 times) and females (1.66 times) of the selected populations survived under cold shock conditions relative to their controls. After being subjected to heat shock, the selected population’s egg viability and mating frequency increased by 0.30 times and 0.57 times, respectively, compared to control populations. Additionally, more selected males (0.31 times) and females (0.98 times) survived under heat shock conditions compared to the control populations. Desiccation resistance slightly increased in the females of the selected populations relative to their control, but we observed no change in the case of males. Starvation resistance decreased in males and females of the selected populations compared to their controls.Our findings suggest that the increased resistance to cold shock correlates with increased tolerance to heat stress, but this evolved resistance comes at a cost, with decreased tolerance to starvation.

Background: The theory of trade-off suggests that limited resources should lead to trade-off in resource intensive traits such as, immunity related and sexually selected traits in males. Alternatively, sexual exaggerations can also act as an honest indicator of underlying immunocompetence, leading to positive correlations between these traits. Evidences in support of either hypothesis in invertebrates is equivocal. Whereas several studies have addressed this question, few have used naturally occurring pathogens and realized post infection realized immunity (e.g., survivorship) to assay the fitness correlations between these two sets of traits. Results: Adopting an experimental evolution approach, we evolved replicate populations of Drosophila melanogaster under (high and low) sexual selection regimes for over a hundred generations and found the following in virgin and mated males in three separate assays: a. Post infection survivorship against two natural pathogens - Pseudomonas entomophila (Pe) and Staphylococcus succinus (Ss): Mated males survived better against Pe, but were no different than virgins against Ss. b. Bacterial clearance ability against a third natural pathogen Providencia rettgeri (Pr): Mated males had significantly lower CFUs than virgins. However, sexual selection history had no effect on realized immunity of either virgin or mated males. Conclusion: We show that while mating can affect realized immunity in a pathogen specific way, sexual selection did not affect the same. The results highlight that complex polygenic traits such as immunity and reproductive traits not necessarily evolve following a binary trade-off model. We also stress the importance natural pathogens while studying sexual selection-immunity correlations.

Immunity and reproduction are two important processes that affect fitness of an organisms. Sexual activity has been previously shown to determine the degree to which a population is able to survive various infections. While many studies have demonstrated a trade-off between immune function and reproduction, many studies have found synergistic relation between the two fitness determinants. Besides it is generally hypothesised that sexes may differ in immunity due to relative cost they incur during reproduction with males losing in immunity to rather increase their reproductive success. In this study, we test the effect of immune function on the survival of mated and virgin replicates of a large outbred baseline D. melanogaster population that was infected with four different bacterial infections. We find enhanced survival in mated flies than virgin flies in response to all four bacterial infections across all replicates. While investigating sexual dimorphism in immune function, we find no difference in sexes in their ability to survive the imposed bacterial infections. Synergistic interaction between reproduction and immunity may exist if it improves Darwinian fitness of either sexes of a population under selection, and are not necessarily limited by each other due to trade-off over finite resources.

The environment experienced by individuals during their juvenile stages has an impact on their adult stages. In holometabolous insects like Drosophila melanogaster, most of the resource acquisition for adult stages happens during the larval stages. Larval-crowding is a stressful environment, which exposes the larvae to scarcity of food and accumulation of toxic waste. Since adult traits are contingent upon larval stages, in larval-crowding like conditions, adult traits are prone to get affected. While the effect of resource limited, poor-developmental environment on adult immune response has been widely studied, the effect of adaptation to resource-limited developmental environment has not been studied, therefore in this study we assayed the evolution of ability to survive infection in adult stages as a correlated response to adaptation to larval crowding environments. Using four populations of Drosophila melanogaster adapted to larval crowding for 240 generations and their respective control populations, we show that populations adapted to larval crowding show an improved and evolved post-infection survivorship against a gram-negative bacteria Pseudomonas entomophila. Whereas, against a gram-positive bacteria Enterococcus faecalis, no difference in post-infection survivorship was observed across control and selected populations. In this study, we report the co-related evolution of pathogen-specific increased survivorship post-infection in populations of Drosophila melanogaster as a result of adaptation to larval crowding environment.

Drosophila melanogaster is an emerging model system for the study of evolutionary ecology of immunity. However, a large number of studies have used non natural pathogens as very few natural pathogens have been isolated and identified. Our aim was to isolate and characterize natural pathogen/s of D. melanogaster . A bacterial pathogen was isolated from wild caught Drosophila spp., identified as a new strain of Staphylococcus succinus subsp. succinus and named PK-1. This strain induced substantial mortality (36–62%) in adults of several laboratory populations of D. melanogaster . PK-1 grew rapidly within the body of the flies post infection and both males and females had roughly same number of colony forming units. Mortality was affected by mode of infection and dosage of the pathogen. However mating status of the host had no effect on mortality post infection. Given that there are very few known natural bacterial pathogens of D. melanogaster and that PK-1 can establish a sustained infection across various outbred and inbred populations of D. melanogaster this new isolate is a potential resource for future studies on immunity.

The ability of interlocus sexual conflict to facilitate reproductive isolation is widely anticipated. However, very few experimental evolutionary studies have convincingly demonstrated the evolution of reproductive isolation due to sexual conflict. Recently a study on replicate populations of Drosophila melanogaster under differential sexual conflict found that divergent mate preference evolved among replicate populations under high sexual conflict regime. The precopulatory isolating mechanism underlying such divergent mate preference could be sexual signals such as cuticular hydrocarbons since they evolve rapidly and are involved in D. melanogaster mate recognition. Using D. melanogaster replicates used in the previous study, we investigate whether cuticular hydrocarbon divergence bears signatures of sexually antagonistic coevolution that led to reproductive isolation among replicates of high sexual conflict regime. We found that D. melanogaster cuticular hydrocarbon profiles are sexually dimorphic. Although replicate populations under high sexual conflict displayed assortative mating, we found no significant differences in the cuticular hydrocarbon profile between the high and low sexual conflict regimes. Instead we find cuticular hydrocarbon divergence patterns to be suggestive of the Buridan’s Ass regime which is one of the six possible mechanisms to resolve sexual conflict. Sexual selection that co-vary between populations under high and low sexual conflict regimes may also have contributed to the evolution of cuticular hydrocarbons. This study indicates that population differentiation as a result of cuticular hydrocarbon divergence cannot be credited to sexual conflict despite high sexual conflict regime evolving divergent cuticular hydrocarbon profiles.

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.

In holometabolous animals such as Drosophila melanogaster, larval crowding can affect a wide range of larval and adult traits. Adults emerging from high larval density cultures have smaller body size and increased mean life span compared to flies emerging from low larval density cultures. Therefore, adaptation to larval crowding could potentially affect adult longevity as a correlated response. We addressed this issue by studying a set of large, outbred populations of D. melanogaster, experimentally evolved for adaptation to larval crowding for 83 generations. We assayed longevity of adult flies from both selected (MCUs) and control populations (MBs) after growing them at different larval densities. We found that MCUs have evolved increased mean longevity compared to MBs at all larval densities. The interaction between selection regime and larval density was not significant, indicating that the density dependence of mean longevity had not evolved in the MCU populations. The increase in longevity in MCUs can be partially attributed to their lower rates of ageing. It is also noteworthy that reaction norm of dry body weight, a trait probably under direct selection in our populations, has indeed evolved in MCU populations. To the best of our knowledge, this is the first report of the evolution of adult longevity as a correlated response of adaptation to larval crowding.

The theory of trade-off suggest that limited resources should lead to trade-off in resource intensive traits such as immunity related and sexually selected traits in males. Alternatively, sexual exaggerations can also act as an honest indicator of underlying immunocompetence, leading to positive correlations between these traits. Several studies have addressed this question using experimental evolution. However, they have rarely used ecologically relevant pathogens and fitness measurement (e.g., measuring post-infection survivorship) to find correlations between sexual selection and immunity. Here we attempt to address this caveat by evolving populations of Drosophila melanogaster under differential sexual selection. After more than hundred generations, we infected virgin and mated males from each population with three pathogenic bacteria: Pseudomonas entomophila (Pe), Staphylococcus succinus (Ss) and Providentia rettgeri (Pr). Fitness was measured as either post-infection survivorship (Pe and Ss) or bacterial clearance ability (Pr). Contrary to expectations, sexual selection had no evolutionary effect on male fitness against any of the pathogens. Moreover, mating had a beneficial effect against Pe and Pr, but no effect against Ss, suggesting pathogen specific phenotypic correlations between mating and immunity. Following these results, we discuss the significance of using ecologically relevant pathogens and quantifying host fitness while studying sexual selection-immunity correlations.

A number of studies have documented the evolution of female resistance to mate-harm in response to the alteration of intersexual conflict in the populations. However, the life-history consequence of such evolution is still a subject of debate. In this study, we subjected replicate populations of Drosophila melanogaster to different levels of sexual conflict (generated by altering the operational sex ratio) for over 45 generations. Our results suggest that females from populations experiencing higher level of intersexual conflict evolved increased resistance to mate-harm, in terms of both longevity and progeny production. Females from the populations with low conflict were significantly heavier at eclosion and were more susceptible to mate-harm in terms of progeny production under continuous exposure to the males. However, these females produced more progeny upon single mating and had significantly higher longevity in absence of any male exposure-a potential evidence of trade-offs between resistance-related traits and other life-history traits, such as fecundity and longevity. We also report tentative evidence, suggesting an increased male cost of interacting with more resistant females.

Given the non-trivial cost of reproduction for males and substantial variation in female quality, males have been predicted to show mating bias as an evolved strategy. Using a large outbred population of Drosophila melanogaster, we test this prediction and show that males may adaptively bias their mating effort in response to the infection status of females. Given a simultaneous choice between females infected with pathogenic bacteria and sham infected females, males preferentially mated with the latter, who had a higher reproductive output compared to infected females. This may provide evidence for pre-copulatory male mate choice. Assessment of the reproductive behaviour ensured that the observed pattern of mating bias was not due to differences in receptivity between females infected with pathogenic bacteria and sham infected females. Further, there was no evidence for post-copulatory male mate choice measured in terms of copulation duration.

In recent years, fairly far-reaching claims have been repeatedly made about how niche construction, the modification by organisms of their environment, and that of other organisms, represents a vastly neglected phenomenon in ecological and evolutionary thought. The proponents of this view claim that the niche construction perspective greatly expands the scope of standard evolutionary theory and that niche construction deserves to be treated as a significant evolutionary process in its own right, almost at par with natural selection. Claims have also been advanced about how niche construction theory represents a substantial extension to, and re-orientation of, standard evolutionary theory, which is criticized as being narrowly gene-centric and ignoring the rich complexity and reciprocity of organism-environment interactions. We examine these claims in some detail and show that they do not stand up to scrutiny. We suggest that the manner in which niche construction theory is sought to be pushed in the literature is better viewed as an exercise in academic niche construction whereby, through incessant repetition of largely untenable claims, and the deployment of rhetorically appealing but logically dubious analogies, a receptive climate for a certain sub-discipline is sought to be manufactured within the scientific community. We see this as an unfortunate, but perhaps inevitable, nascent post-truth tendency within science.

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 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) interaction 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.

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.