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Duneau, D.

Publications and source records attributed to Duneau, D..

10 recordsLinked to original sources

Seminal fluid proteins can mitigate sexual conflict: the case of remating in insects

Males during mating never transfer just sperm; to the best of our knowledge, they always deliver a rich seminal fluid as well. The proteins in the seminal fluid have an important sperm supporting role, but they also cause changes in the female physiology and can impose a mating cost. The associated costs and delay in the time of remating, lead to the view that those proteins evolved primarily due to sexual conflict and delay female remating beyond the optimal rate. To examine the role of seminal fluid proteins in sexual conflict we use a mathematical model of reproductive physiology, informed by the accumulated knowledge on Drosophila melanogaster. In accordance with the theory, we find that males always benefit from inducing longer remating intervals in females. But, we also find that this conflict is reduced when female reproduction is regulated by the male proteins. Without seminal fluid proteins females have a single, well-defined, optimal remating rate. However, when seminal proteins are used to regulate females reproduction, females can reach the same offspring production for a range of mating intervals. This wider range of possible remating times could provide females with a buffer against uncertain mating opportunity. It could also allow females to be more selective on male quality, by reducing the cost associated with delaying remating. Our results suggest that, while there is a conflict over the remating rate, seminal fluid proteins reduce its intensity, highlighting their role in aligning the interests of both sexes.

evolutionary biology↗

The role of fecundity dynamics and time of injury for femalereproductive fitness

Animals have a wide range of reproductive strategies and change how they produce offspring as a function of their age, environment, risk of predation or starvation, and as a result of trade-offs with other life history traits. In turn, these temporal patterns of reproduction, or fecundity dynamics, will determine how vulnerable the animal is to many of the same factors that shaped the dynamics in the first place. In this study, we tested how individual fecundity dynamics influence vulnerability of female fecundity to the deleterious environmental factors. We injured Drosophila melanogaster females at various moments during periods before and after mating. Injuries are prevalent in nature and provide a punctuated stimulus, making them particularly well suited to study their connection with the dynamics of reproduction. Our aim was to determine periods of vulnerability and impact of wounds on female fitness resulting from the change. The observed fecundity dynamics exhibited a high early peak in offspring production, suggesting that early after mating females might be particularly vulnerable to environmental conditions. However, females produced the same number of offspring, regardless of the time of injury, suggesting that fitness of female Drosophila is robust to wounds inflicted under laboratory conditions.

evolutionary biology↗

Different ways to die: harnessing variation in Drosophila reveals loss of tolerance and resistance over age and sex-specific association between infection susceptibility and lifespan

It is widely accepted that susceptibility to infection increases with age. The reason often invoked is the dysregulation of the immune system, which is both cause and consequence of ageing. However, we do not all age in the same way, and increased susceptibility may not be solely due to immune dysregulation affecting resistance to infection. There are many possible ways to make a host less tolerant to infection by dysregulating key physiological or metabolic processes. We hypothesised that the increase in susceptibility to infection over age can be linked to both immune ageing and decreased tolerance, and importantly, that it will depend on genotype and sex of the host. We assessed susceptibility to Gram-negative bacterial challenge in both sexes in 22 Drosophila isolines at young and old ages, and leveraged variation between genotypes to investigate how frequently an increase in susceptibility to infection was more associated with a decline in resistance or disease tolerance mechanisms. To achieve this, we assessed pathogen load to report on host immune decline. Strikingly, in most cases, greater infection susceptibility at old age was driven by reduced tolerance, although we also frequently identify cases that suffered bona fide immunosenescence, e.g. impaired resistance. We screened across bacterial pathogens during systemic and oral infections and found sex-specific signatures in survival in young and old individuals, but increased susceptibility with age occurred in both sexes. Pairing infection survival with lifespan data, we find that transcending genotype variation, susceptibility at old age predicts lifespan in males only, regardless of the existence or direction of sex bias in longevity. This work highlights that increased infection susceptibility is an early-arising ageing phenotype that occurs in both sexes, but only predicts lifespan in males, paralleling burgeoning evidence in mammals for male-biased effects of age on infection and its connection with mortality. Our data support a model where infection susceptibility increases with age following the same multiplicative pattern as organismal mortality, with existing failures making new failures more consequential. We propose that the term "immunosenescence" be used specifically to describe proven dysregulation of immune tissue resistance mechanisms. We argue that to fully understand the drivers of age-related susceptibility to infection, it is essential to consider genotype, sex, and their interaction, as well as the dysregulation of non-immune functions that influence the ability to control pathogens.

immunology↗

Wound-induced eyespots on butterfly wings at the intersection of immune response and pigmentation development

Butterfly eyespots are striking examples of evolutionary novelty arising through the repurposing of ancestral genetic pathways, including pathways involved in wound healing. Given the activation of the immune system during wound healing, and the known links between immunity and pigmentation, we hypothesized that the immune response triggered by wounding contributes to the formation of wound-induced ectopic eyespots on butterfly wings. We tested this hypothesis by wounding the wings of Bicyclus anynana pupae and modulating immune challenge levels with application of varying quantities of heat-killed bacteria. These led to up-regulation of defense-related genes in the wounded wing as well as in the contralateral non-wounded wing. Immune activation did not affect the likelihood of ectopic eyespot formation, but it did significantly influence the extent of pigmentation changes around injury sites: stronger immune activation produced larger ectopic eyespots. This effect was localized to the treated wing and did not affect contralateral, control wound-induced eyespots. Additionally, stronger immune challenges led to smaller overall wing size and to relatively smaller native eyespots. Our findings reveal that immune activation contributes to the development of wound-induced eyespots and impacts both pigmentation pattern formation and wing size regulation. These results underscore the complex interplay between immune function and developmental processes, and provide new insights into the origins of lineage-specific morphological innovations.

evolutionary biology↗

Sex Differences in Drosophila Intestinal Metabolism Contribute to Sexually Dimorphic Infection Outcome and Alter Gut Pathogen Virulence

Sexual dimorphism in infection outcomes is a pervasive phenomenon, the underlying mechanisms of which remain incompletely understood. Here, utilizing Pseudomonas entomophila intestinal infection in Drosophila, we demonstrated that sex differences in intestinal redox processes contribute to female bias in susceptibility to gut infection. Female inability to overcome excessive pathogen-induced oxidative stress results in defecation blockage, pathogen persistence, and host death. Male flies exhibit increased carbohydrate metabolism and pentose phosphate pathway activity - a key antioxidant defense system. This allows males to withstand oxidative stress-induced defecation blockage and clear the pathogen from the intestine, resulting in survival. Additionally, P. entomophila showed increased expression of several virulence factors, including RNA-binding protein Hfq, in the female gut, contributing to female-biased virulence of P. entomophila. Thus, the effect of the gut metabolic environment on host defenses and pathogen virulence determines the sex differences in intestinal infection outcomes. HighlightsIntestinal transit of gut pathogen contributes to sexually dimorphic susceptibility to Drosophila gut infection. Male bias in PPP favors pathogen clearance and recovery post-infection. P. entomophila reacts differently to female gut environment, where higher levels of Hfq might contribute to virulence/lethality. O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=200 SRC="FIGDIR/small/655590v1_ufig1.gif" ALT="Figure 1"> View larger version (61K): org.highwire.dtl.DTLVardef@1d6d36borg.highwire.dtl.DTLVardef@d24f2aorg.highwire.dtl.DTLVardef@14b4ed1org.highwire.dtl.DTLVardef@123b46c_HPS_FORMAT_FIGEXP M_FIG C_FIG

immunology↗

Can seminal fluid proteins be honest signals of sperm availability?

Seminal fluid proteins (Sfps) are produced by males, yet they have significant effects on female physiology and behaviour. Sfps are often viewed as a mechanism for males to manipulate female reproductive behaviours, but despite many studies identifying their varied effects and their molecular underpinnings, the ways males and females use Sfps remain unclear. In the most studied case of Drosophila melanogaster particular peptides within the seminal fluid have been identified to guide female reproduction: sex peptide (SP, Acp70A) is known to induce changes in egg production, oviposition and remating and is attached to sperm and continuously supplied for days after mating, while ovulation inducing peptide, ovulin (Acp26Aa), is a free peptide with only short term effects after mating. Using a biologically informed model we show how these peptides can synchronize sperm and egg release, hence reducing the number of unfertilized eggs a female lays. We further show that the exhaustion of SP might be the key signal of this synchronization. Finally, we demonstrate that sexual conflict over the regulation of female reproductive physiology by Sfps should be limited, with the primary conflict probably centring around the regulation of remating behaviour.

evolutionary biology↗

Estimation of the propensity for sexual selection in a cyclical parthenogen

Cyclical parthenogenesis is a widespread reproductive strategy in which organisms go through one or multiple rounds of clonal reproduction before sexual reproduction. Because sexual reproduction is typically less common than parthenogenesis in populations of the planktonic cladoceran Daphnia magna, it is not frequently studied. Here we examine the sexual process of D. magna and its relation to sexual selection in Daphnia rockpool populations by observing natural mating in these shallow habitats where sex generally occurs throughout the summer. Although microsatellite markers were found to reveal no evidence of disassortative mating or, thus, of inbreeding avoidance, body length and infection status did reveal assortative mating, suggesting sexual selection to act. When two males mated with a single female, the larger male was observed to remain longer, possibly giving it an advantage in sperm competition. Indirect evidence points at the brood pouch as the likely site of fertilization and thus, sperm competition. Sperm length was as variable within ejaculates as it was among males from different populations. Our data provide firm evidence that sexual selection is present in this species, most likely manifesting itself through a combination of female choice and male-male competition.

evolutionary biology↗

Signatures of insecticide selection in the genome of Drosophila melanogaster.

Resistance to insecticides has evolved in multiple insect species, leading to increased application rates and even control failures. Understanding the genetic basis of insecticide resistance is fundamental for mitigating its impact on crop production and disease control. We performed a GWAS approach with the Drosophila Genetic Reference Panel (DGRP) to identify the mutations involved in resistance to two widely used classes of insecticides: organophosphates (OPs, parathion) and pyrethroids (deltamethrin). Most variation in parathion resistance was associated with mutations in the target gene Ace, while most variation in deltamethrin resistance was associated with mutations in Cyp6a23, a gene encoding a detoxification enzyme never previously associated with resistance. A \"nested GWAS\" further revealed the contribution of other loci: Dscam1 and trpl were implicated in resistance to parathion, but only in lines lacking Wolbachia. Cyp6a17, the paralogous gene of Cyp6a23, and CG7627, an ATP-binding cassette transporter, were implicated in deltamethrin resistance. We observed signatures of recent selective sweeps at all of these resistance loci and confirmed that the soft sweep at Ace is indeed driven by the identified resistance mutations. Analysis of allele frequencies in additional population samples revealed that most resistance mutations are segregating across the globe, but that frequencies can vary substantially among populations. Altogether, our data reveal that the widely used OP and pyrethroid insecticides imposed a strong selection pressure on natural insect populations. However, it remains unclear why, in Drosophila, resistance evolved due to changes in the target site for OPs, but due to a detoxification enzyme for pyrethroids.\n\nArticle summaryInsecticides are widely used to control pests and insect vectors of disease. In response to the strong selection pressure exerted by insecticides, resistance has evolved in most insect species. We identified few genes present in several Drosophila melanogaster natural populations implicated in the evolution of resistance against two insecticides widely used today. We identified primary and secondary genes involved in the resistance. Surprisingly, resistance evolved in the target site for one insecticide, but was associated to changes in a novel detoxification enzyme for the other insecticide.

evolutionary biology↗

Genetic basis of thermal plasticity variation in Drosophila melanogaster body size

Body size is a quantitative trait that is closely associated to fitness and under the control of both genetic and environmental factors. While developmental plasticity for this and other traits is heritable and under selection, little is known about the genetic basis for variation in plasticity that can provide the raw material for its evolution. We quantified genetic variation for body size plasticity in Drosophila melanogaster by measuring thorax and abdomen length of females reared at two temperatures from a panel representing naturally segregating alleles, the Drosophila Genetic Reference Panel (DGRP). We found variation between genotypes for the levels and direction of thermal plasticity in size of both body parts. We then used a Genome-Wide Association Study (GWAS) approach to unravel the genetic basis of inter-genotype variation in body size plasticity, and used different approaches to validate selected QTLs and to explore potential pleiotropic effects. We found mostly \"private QTLs\", with little overlap between the candidate loci underlying variation in plasticity for thorax versus abdomen size, for different properties of the plastic response, and for size versus size plasticity. We also found that the putative functions of plasticity QTLs were diverse and that alleles for higher plasticity were found at lower frequencies in the target population. Importantly, a number of our plasticity QTLs have been targets of selection in other populations. Our data sheds light onto the genetic basis of inter-genotype variation in size plasticity that is necessary for its evolution.\n\nSignificance StatementThe environmental conditions under which development takes place can affect developmental outcomes and lead to the production of phenotypes adjusted to the environment adults will live in. This developmental plasticity, which can help organisms cope with environmental heterogeneity, is heritable and under selection. Plasticity can itself evolve, a process that will be partly dependent on the available genetic variation for this trait. Using a wild-derived D. melanogaster panel, we identified DNA sequence variants associated to variation in thermal plasticity for body size. We found that these variants correspond to a diverse set of gene functions. Furthermore, their effects differ between body parts and properties of the thermal response, which can, therefore, evolve independently. Our results shed new light onto a number of key questions about the long discussed genes for plasticity.

evolutionary biology↗

Complex effects of day and night temperature fluctuations on thermally plastic traits in an experimental model of adaptive seasonal plasticity.

BackgroundChanges in development in response to seasonally variable environments can produce phenotypes adjusted to fluctuating seasonal conditions and help organisms cope with temporal heterogeneity. In contrast to what happens in natural situations, experimental studies of developmental plasticity typically use environmental factors held constant during development, precluding assessment of potential environment-by-environment interaction effects.\n\nResultsWe tested effects of circadian fluctuations in temperature on a series of thermally plastic traits in a model of adaptive seasonal plasticity, the butterfly Bicyclus anynana. Comparing phenotypes from individuals reared under two types of fluctuations (warmer days with cooler nights, and cooler days with warmer nights) and those reared under a constant temperature of the same daily average allowed us to identify complex patterns of response to day and night temperatures. We found evidence of additive-like effects (for body size), but also different types of \"dominance\"-type effects where one particular period of the light cycle (for development time) or one particular extreme temperature (for eyespot size) had a relatively larger contribution to phenotype expression. We also gathered evidence against the hypothesis that thermal plasticity in development time drives thermal plasticity in other traits.\n\nConclusionsCombined effects of fluctuating day and night temperatures include additive-like effects as well as different types of environmental-dominance interaction effects. Differences between plastic traits reveal independent responses to temperature, and possible independent assessment of temperature conditions. Our study underscores the importance of understanding how organisms integrate complex environmental information towards a complete understanding of natural phenotypic variation and of the potential impact of environmental change thereon.

evolutionary biology↗