Sleep is a deeply conserved and universal feature of many organisms, but the specific biological mechanisms remain poorly understood. We seek to understand why young animals sleep more than mature adult animals, as sleep is believed to play a specific role in brain development during the juvenile stage. Drosophila Melanogaster is a powerful model organism used to study genes involved in sleep. Studies show that the dopaminergic cells that synapse onto the sleep-promoting dorsal fan shaped body neurons of flies inhibit sleep output, thus promoting arousal. These dopamine neurons are less active in young flies, causing a more active sleep center. We aim to identify what controls this change in dopamine activity throughout fly maturation. Using preliminary results from single-cell RNA sequencing of changes in gene expression over the lifetime of a fly, we manipulated the expression of genes that are more highly expressed in the dopaminergic neurons of mature flies and observed their sleep behavior through a behavioral screen using the GAL4-UAS system. “Hits” were defined as RNAi lines that increased sleep in mature adult flies. A number of hits from the screen were mitochondrial genes involved in the electron transport chain. When the ND-51 gene, a component of Complex I of the electron transport chain, was knocked down, it caused increased sleep in mature flies. Looking more carefully at other genes involved in Complex I, we found several genes whose knockdown also caused an increased sleep phenotype. Future work will focus on the biological significance of Complex I as well as the role of ATP production in sleep ontogeny