Reduced insulin signaling promotes germline stem cell maintenance under P-element hybrid dysgenesis

Transposable elements (TEs) are selfish mobile DNA segments that proliferate throughout the host genome by replicating in gamete nuclei, thus allowing for vertical transmission to progeny. While often suppressed by the host, the consequences of unchecked transposition are severe, inducing deleterious mutations and disrupting the function of gametes. In the case of the P-element, a DNA transposon of Drosophila melanogaster, unregulated transposition results in atrophied ovaries that contain no germline cells. DNA damage from the P-element is hypothesized to impair germline stem cells (GSCs) in Drosophila ovaries, resulting in their permanent loss. We sought to uncover the mechanisms that promote GSC loss in the presence of P-element activity by manipulating the differentiation signals that a GSC receives. In particular, decreasing differentiation signals may suppress atrophy by stabilizing GSCs in the niche. To test this hypothesis we selected 16 genes involved GSC differentiation, and reduced their expression in dysgenic germlines using GAL4-UAS mediated RNAi. Knock-down of two genes, raptor and chico, resulted in germline rescue in dysgenic ovaries. Chico and Raptor are components of the insulin signaling pathway, which promotes the G2/M transition in GSCs. Our observations therefore suggest that G2 arrest may be critical for the recovery of GSCs from P-element induced DNA-damage.