Recovery from cold-induced reproductive dormancy is regulated by temperature-dependent AstC signaling.

Animals have evolved a variety of behaviors to cope with adverse environmental conditions. Similar to other insects, the fly, Drosophila melanogaster, responds to sustained cold by reducing its metabolic rate and arresting its reproduction. Here, we show that a subset of dorsal neurons (DN3s) that express the neuropeptide allatostatin C (AstC) facilitates recovery from cold-induced reproductive dormancy. The activity of AstC-expressing DN3s, as well as AstC peptide levels, are suppressed by cold. Cold temperature also impacts AstC levels in other Drosophila species and mosquitoes, Aedes aegypti, and Anopheles stephensi. The stimulatory effect of AstC on egg production is mediated by cholinergic AstC-R2 neurons. Our results demonstrate that DN3s coordinate female reproductive capacity with environmental temperature via AstC signaling. AstC/AstC-R2 is conserved across many insect species and their role in regulating female reproductive capacity makes them an ideal target for controlling the population of agricultural pests and human disease vectors.