Abstract

Transposable elements (TEs) are genomic parasites that proliferate within host genomes, and can also invade new species. The P-element, a DNA-based transposable element, recently invaded two Drosophila species: D. melanogaster in the 20th century, and D. simulans, in the 21st. In both species, lines collected before the invasion are susceptible to ‘hybrid dysgenesis’, a syndrome of abnormal phenotypes that are due to P-element inflicted DNA damage. In D. melanogaster, lines collected after the invasion have evolved a maternally acting mechanism that suppresses the effects of the P-element and therefore hybrid dysgenesis. Extensive work has shown that PIWI-interacting small RNAs (piRNAs) are a key factor suppressing P-element induced hybrid dysgenesis. However, most of these studies were performed using lines collected many generations after the initial P-element invasion. In this thesis, I study lines of D. simulans collected early and late in the invasion of the P-element in that species. Similar to D. melanogaster, late in the invasion D. simulans shows abundant P-element derived piRNAs. Lines collected early in the invasion show substantial variation tolerance to the P-element. Surprisingly, however, these lines show no correlation between tolerance to P- element damage and expression of maternal P-element piRNAs, or other known factors influencing hybrid dysgenesis, suggesting mechanisms contribute to P-element suppression prior to the evolution of piRNA suppression. In addition to that, I identify piRNA-producing loci, piRNA clusters, in D. simulans.

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