When the two sexes of anisogamous species maximize their fitness in different ways , this difference creates a sexual conflict, in which traits favored in one sex are not favored in the other . There are two types of sexual conflict. Intralocus sexual conflict occurs when the targets of selection are alleles at the same loci in both sexes . Interlocus sexual conflict, which is less well-understood, involves alleles at separate loci . Under interlocus sexual conflict, one sex evolves traits that improve its reproductive success at the expense of the other. In turn, this generates selection on the other sex to resist the effects of these traits. The outcome is thought to be an evolutionary arms race between the two sexes known as sexually antagonistic coevolution (SAC) .
There are two major limitations to studying SAC. First, most studies on SAC rely on phenotypic data alone. This means that compelling genomic evidence for how SAC evolves is lacking . Second, there is a historical disparity in research focus: much more attention has been paid to the genetic mechanisms underlying male trait evolution than female trait evolution . This is another example of the well-known disparity between studies of males and females in medicine and biology [6; 7], including in terms of reproductive tract and genital evolution [5; 8]. To establish the importance of female evolution for driving SAC, my dissertation focused on the genetic mechanisms behind female resistance to male-induced harm.
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Three Aims of Dissertation
- Quantify variation in female resistance among different inbred lines and identify genomic regions associated with this variation.
- A. Quantify variation in male harm among different inbred lines.
- B. Quantify variation in female resistance among different inbred lines.
- C. Perform genome-wide association study (GWAS) for female resistance using data from 1B.
- Evolve a population of females while preventing males from coevolving, and use both phenotypic and genetic data to determine if and how females evolved a higher level of resistance. CANCELLED DUE TO COVID-19.
- Analyze the effects of genes implicated in both Aim 1
and Aim 2to determine if they are truly involved in female’s resistance, and if so, to what extent.
Drosophila melanogaster exhibits extensive sexual conflict. Males have
evolved proteins in their seminal fluid (SFPs) that increase their own fitness [9; 10], but decrease the lifespan  and lifetime reproductive success  of their female partners. Much of the research surrounding sexual conflict in D. melanogaster has focused largely on males, including the identification of numerous SFPs [10; 13] and quantification of genetic variation for male harm [14; 15].
The female side of this dynamic, however, has not received as much attention. Some studies show that some females are more resistant to male harm than others [14; 16], and that females can evolve resistance to higher mating rates [17; 18]. It is unclear whether female resistance evolves in response simply to harassment due to mating rate, a behavior, or physiologically based male harm. Molecular evolution studies show that genes in the female reproductive tract are under positive directional selection [19; 20]. While this is consistent with the evolution of female resistance, it is not definitive, because evidence of positive selection at this level is not evidence about the agent of selection. There is also evidence that a variety of genes can influence female fecundity  and post-mating behavior [22; 23], but it is not known whether these genes are involved in female resistance to male harm. The most comprehensive genomic study to date is a genome-wide association study  that examined intra– rather than interlocus sexual conflict. This study did not specifically measure female resistance and obtained results that are contradictory to many theoretical predictions [25; 26].
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