As Drosophila shares a significant number of genes with humans, studying Drosophila can provide insights into sleep regulation, a process that is not well understood. In Drosophila, the insomniac (inc) gene encodes a putative adaptor protein for the Cullin-3 ubiquitin ligase complex. A nonfunctional Inc protein results in fragmented sleep and excess neurons in the mushroom body, a brain region important for sleep. This study intends to determine whether C-terminal Inc mutants can successfully rescue the mushroom body defects caused by a null inc mutation. A prior rescue experiment indicated that full-length Inc protein rescued sleep in inc mutants to wild-type levels; however, C-terminal Inc mutants could not rescue sleep. To evaluate if C-terminal Inc mutants could rescue the mushroom body defects of inc mutants, a fly cross was conducted between inc mutants and C-terminal mutants via the GAL4/UAS system. From the resulting progeny, the brains of adult male Drosophila were dissected and visualized through immunohistochemistry and confocal microscopy. Our results suggest that transgenic expression of full-length Inc protein results in a normal mushroom body, but further experimentation is needed to confirm this result. The effects of C-terminal Inc mutants on mushroom body anatomy also require further investigation.
