Mimi Shirasu-Hiza’s laboratory investigates the role of circadian-regulated physiologies such as innate immunity (including the function of glia, or non-neuronal cells, of the brain), metabolism and sleep in disease progression using the genetically tractable model organism Drosophila melanogaster. Disease models that Shirasu-Hiza studies in Drosophila include bacterial infection, aging and fragile X syndrome, the most common monogenic cause of autism in humans. The study of fragile X syndrome and autism is a growing focus of the laboratory. In studying the circadian-dysregulated fragile X model dFmr1 mutant, her laboratory identified defects in phagocytosis mediated by both systemic immune cells and glia, both during development and in adulthood. Through collaboration with Carol Mason’s laboratory, they are now extending this investigation into mice.