Sexual conflict drives male manipulation of female postmating responses in Drosophila melanogaster.

In many animals, females respond to mating with changes in physiology and behavior that are triggered by molecules transferred by males during mating. In Drosophila melanogaster, proteins in the seminal fluid are responsible for important female postmating responses, including temporal changes in egg production, elevated feeding rates and activity levels, reduced sexual receptivity, and activation of the immune system. It is unclear to what extent these changes are mutually beneficial to females and males or instead represent male manipulation. Here we use an experimental evolution approach in which females are randomly paired with a single male each generation, eliminating any opportunity for competition for mates or mate choice and thereby aligning the evolutionary interests of the sexes. After >150 generations of evolution, males from monogamous populations elicited a weaker postmating stimulation of egg production and activity than males from control populations that evolved with a polygamous mating system. Males from monogamous populations did not differ from males from polygamous populations in their ability to induce refractoriness to remating in females, but they were inferior to polygamous males in sperm competition. Mating-responsive genes in both the female abdomen and head showed a dampened response to mating with males from monogamous populations. Males from monogamous populations also exhibited lower expression of genes encoding seminal fluid proteins, which mediate the female response to mating. Together, these results demonstrate that the female postmating response, and the male molecules involved in eliciting this response, are shaped by ongoing sexual conflict.

Divergence in sex peptide-mediated female post-mating responses in Drosophila melanogaster.

Transfer and receipt of seminal fluid proteins crucially affect reproductive processes in animals. Evolution in these male ejaculatory proteins is explained with post-mating sexual selection, but we lack a good understanding of the evolution of female post-mating responses (PMRs) to these proteins. Some of these proteins are expected to mediate sexually antagonistic coevolution generating the expectation that females evolve resistance. One candidate in Drosophila melanogaster is the sex peptide (SP) which confers cost of mating in females. In this paper, we compared female SP-induced PMRs across three D. melanogaster wild-type populations after mating with SP-lacking versus control males including fitness measures. Surprisingly, we did not find any evidence for SP-mediated fitness costs in any of the populations. However, female lifetime reproductive success and lifespan were differently affected by SP receipt indicating that female PMRs diverged among populations. Injection of synthetic SP into virgin females further supported these findings and suggests that females from different populations require different amounts of SP to effectively initiate PMRs. Molecular analyses of the SP receptor suggest that genetic differences might explain the observed phenotypical divergence. We discuss the evolutionary processes that might have caused this divergence in female PMRs.

Precopulatory but not postcopulatory male reproductive traits diverge in response to mating system manipulation in Drosophila melanogaster.

Competition between males creates potential for pre- and postcopulatory sexual selection and conflict. Theory predicts that males facing risk of sperm competition should evolve traits to secure their reproductive success. If those traits are costly to females, the evolution of such traits may also increase conflict between the sexes. Conversely, under the absence of sperm competition, one expectation is for selection on male competitive traits to relax thereby also relaxing sexual conflict. Experimental evolution studies are a powerful tool to test this expectation. Studies in multiple insect species have yielded mixed and partially conflicting results. In this study, we evaluated male competitive traits and male effects on female costs of mating in Drosophila melanogaster after replicate lines evolved for more than 50 generations either under enforced monogamy or sustained polygamy, thus manipulating the extent of intrasexual competition between males. We found that in a setting where males competed directly with a rival male for access to a female and fertilization of her ova polygamous males had superior reproductive success compared to monogamous males. When comparing reproductive success solely in double mating standard sperm competition assays, however, we found no difference in male sperm defense competitiveness between the different selection regimes. Instead, we found monogamous males to be inferior in precopulatory competition, which indicates that in our system, enforced monogamy relaxed selection on traits important in precopulatory rather than postcopulatory competition. We discuss our findings in the context of findings from previous experimental evolution studies in Drosophila ssp. and other invertebrate species.

Down syndrome cell adhesion molecule 1: testing for a role in insect immunity, behaviour and reproduction.

Down syndrome cell adhesion molecule 1 (Dscam1) has wide-reaching and vital neuronal functions although the role it plays in insect and crustacean immunity is less well understood. In this study, we combine different approaches to understand the roles that Dscam1 plays in fitness-related contexts in two model insect species. Contrary to our expectations, we found no short-term modulation of Dscam1 gene expression after haemocoelic or oral bacterial exposure in Tribolium castaneum, or after haemocoelic bacterial exposure in Drosophila melanogaster. Furthermore, RNAi-mediated Dscam1 knockdown and subsequent bacterial exposure did not reduce T. castaneum survival. However, Dscam1 knockdown in larvae resulted in adult locomotion defects, as well as dramatically reduced fecundity in males and females. We suggest that Dscam1 does not always play a straightforward role in immunity, but strongly influences behaviour and fecundity. This study takes a step towards understanding more about the role of this intriguing gene from different phenotypic perspectives.

Saving ears and kidneys from cisplatin.

Cisplatin is a potent cytostatic drug, whose use is limited by its severe acute and chronic nephro-, oto-, and also peripheral neuro-toxicity. Since transporters are important mediators of specific cellular uptake of many drugs such as cisplatin, their role as possible targets of specific organ protection against undesired cisplatin toxicities is under investigation. Several transporters are able to mediate the movement of cisplatin across the plasma membranes: Copper transporter-1 (Ctr1), copper transporter-2 (Ctr2), P-type copper-transporting ATPases ATP7A and ATP7B, organic cation transporter-2 (OCT2), and multidrug extrusion transporter-1 (MATE1). Some of these transporters are also able to accept other platinum derivatives as substrates. In the present review article, we focus on the role of Ctr1 and OCT2 for cellular uptake of cisplatin and on the possibilities to reduce cisplatin-associated toxicities decreasing cisplatin uptake mediated by these transporters. The ubiquitously expressed Ctr1 seems to be involved in general cisplatin uptake in tumor and normal cells. Conversely, OCT2 expression is restricted to few cells such as renal, cochlear, and nervous cells, while its expression in some tumors seems to be epigenetically down-regulated. For this reason, specific inhibition of OCT2 may be effective in decreasing cisplatin uptake in non-target cells, without compromising its anti-tumoral efficacy, and therefore OCT2 may be the target for a suitable protective therapy.