| In 1982 Donal Hickey, demonstrated that in populations of sexually reproducing organisms, genetic parasites such as transposable elements can invade even if they harm the host. In the past several years it has become clear that a vast immune system evolved within early eukaryotes to ward against these harmful effects. This immune system is known as the RNA interference (RNAi) pathway. Using small interfering RNAs (siRNAs) that are derived from the very same parasitic transcripts, the RNAi pathway is able to target harmful genetic parasites, as well as viruses, for destruction. In this thesis I focus on the forces of selection that act on transposable elements and how hosts defend against these parasites. I also explore how males and females, with different reproductive interests, differ in their strategies for defending their offspring against these parasites.; This thesis comes in four parts. In the first chapter, done in collaboration with Elena Lozovsky, I explore how natural selection may have shaped the distribution of transposable elements within the genome of Drosophila melanogaster . In the second chapter, I develop a statistical test that allows one to test the neutrality of transposable element insertions without assuming that insertion frequencies are at equilibrium. In the third chapter, I provide evidence that in Drosophila virilis, transposable element siRNAs are epigenetically inherited from females, but not males. This observation may explain the long-standing observation that in hybrid dysgenesis syndromes of Drosophila, transposable elements inherited paternally are active, but their activation can be repressed by likely cytoplasmic factors inherited maternally. In the fourth chapter, I develop a mathematical model that suggests that sperm competition may explain this dichotomy. Since males must compete with other males to fertilize female gametes, if there is a cost of maintaining a low mutation rate, natural selection may favor males that produce large numbers of sperm but allow more harmful mutations in their offspring. This may explain the long-standing observation of a higher mutation rate in males. |
