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Authors

Gabriella Yray

Abstract

Sexual conflict is understood as differential optimal reproductive fitness between the sexes of a species, which can lead to an evolutionary arms race between the sexes. Typically,males evolve mechanisms to induce females to mate more often than is optimal, and females are selected to inhibit the effects of male manipulation. This antagonism, known as sexual conflict, has shaped the interactions of virtually all sexual species. Understanding the genetic basis of these conflict-based characteristics is key not only to increasing our understanding of sexual conflict but also to our understanding of the reproductive physiology and behavior of species. Drosophila melanogaster males and females possess a gene that codes for a putative serine endopeptidase, CG18125, which may mediate male sexual conflict mechanisms through influencing female fecundity and fertility. We hypothesized that heightened expression of CG18125 post-mating was due to its defensive purpose toward male manipulation, and that by deactivating the gene’s functionality, we would increase fecundity and fertility as compared to that of normal female serine endopeptidase activity, thereby demonstrating that the gene in females acts as a mediator for male manipulation. Alternatively, we hypothesized that the drastically increased post-mating expression of the gene product may in fact be triggered by males as a way of ensuring an increased level of egg production, meaning that when the gene is absent, female egg production might decrease. In order to acquire this data, we performed a targeted suppression of expression within the female reproductive tract by RNA interference Compromised Mating Responsive Gene in Drosophila ׀ 2 (RNAi), which inhibited serine endopeptidase functionality, and recorded day-to-day egg deposition as well as viability counts for 12 days. Results demonstrated that there was no significant difference for or against fecundity but that experimental disruption of serine endopeptidase activity led to increased fecundity. However, experimental females did show a significant rise in egg production when compared to control females, on the first few days of egg laying. These results show that CG18125 expression does not affect fecundity numbers, but instead that it downregulates fertility. It is possible that CG18125 plays a role in physiological female protection by allotting a balance of egg production, and/or that males prosper from a shorter offspring generation time when the gene does not function correctly.

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