Drosophila melanogaster females undergo reproductive dormancy, or diapause, under conditions of low temperature and short daylight hours. This stage is characterized by non-vitellogenic ovaries, increased lipid stores, decreased senescence, and increased resistance to stress. My study tests whether diapause affects resistance to bacterial pathogens and whether an infection influences entry into diapause. I hypothesize that diapause and immunity are reciprocally connected, with diapause increasing resistance to infection and infection increasing the probability of entry into diapause. I have preliminarily found that D. melanogaster genotypes with higher propensity to enter into diapause sustain decreased pathogen load after infection. Previous studies show that insulin signaling may regulate diapause, and that the Toll signaling pathway of the innate immune response disrupts insulin signaling. Future experiments will determine whether the relationship between immunity and diapause is mediated by regulation of insulin signaling, and what roles the genes regulating diapause or immunity play in regulating the insulin pathway. The results of my study provide the first evidence that, in addition to decreased senescence and increased stress resistance, the diapause state also increases resistance to bacterial infection.