A Role for Maternal Factors in Suppressing Cytoplasmic Incompatibility

are maternally transmitted bacterial endosymbionts, carried by approximately half of all insect species. prevalence in nature stems from manipulation of host reproduction to favor the success of infected females. The best known reproductive modification induced by is referred to as sperm-egg Cytoplasmic Incompatibility (CI). In CI, the sperm of -infected males cause embryonic lethality, attributed to paternal chromatin segregation defects during early mitotic divisions. Remarkably, the embryos of infected females "rescue" CI lethality, yielding egg hatch rates equivalent to uninfected female crosses. Several models have been discussed as the basis for Rescue, and functional evidence indicates a major contribution by CI factors. A role for host contributions to Rescue remains largely untested. In this study, we used a chemical feeding approach to test for CI suppression capabilities by . We found that uninfected females exhibited significantly higher CI egg hatch rates in response to seven chemical treatments that affect DNA integrity, cell cycle control, and protein turnover. Three of these treatments suppressed CI induced by endogenous Ri , as well as an ectopic Mel infection. The results implicate DNA integrity as a focal aspect of CI suppression for different strains. The framework presented here, applied to diverse CI models, will further enrich our understanding of host reproductive manipulation by insect endosymbionts.