Interaction between juvenile hormone and insulin/IGF-like signaling mediates lipid homeostasis during lactation in the tsetse fly, Glossina morsitans. Aaron A. Baumann¹, Joshua B. Benoit², Veronika Michalkova², Paul Mireji³, Geoffrey M. Attardo², John K. Moulton⁴, Thomas G. Wilson⁵, Serap Aksoy². 1) HHMI Janelia Farm Research Campus, Ashburn, VA; 2) School of Public Health, Yale University, New Haven, CT; 3) Department of Biochemistry and Molecular Biology, Egerton University, Njoro, Kenya; 4) Department of Entomology and Plant Pathology, University of Tennessee, Knoxville TN; 5) Department of Evolution, Ecology, and Organismal Biology, Ohio State University, Columbus, OH.

   Juvenile hormone (JH) mediates reproductive maturation in most insects, acting via the bHLH PAS transcription factor MET. The Drosophila genome contains both Met and its paralog Gce, genes with similar function in development but not in reproduction. Similarly, annotation of the tsetse (Glossina morsitans) genome revealed distinct Met and Gce orthologs. Tsetse flies employ viviparous reproduction, in which females nourish a developing intrauterine larva with a protein- and lipid-rich milk secreted from a modified accessory gland. We examined roles for Met, Gce, and insulin signaling (IIS) during the lactating and dry (non-lactating) stages of tsetse pregnancy, using a combination of hormone application and siRNA-mediated gene suppression. Perturbing either the JH or IIS pathway interfered with lipid homeostasis that is critical for tsetse lactation, suggesting JH/IIS interaction in this physiology. Specifically, siRNA reduction of Met but not Gce expression resulted in 1) elevated expression of the lipase bmm, a FOXO target gene, and 2) reduced expression of the class II histone deacetylase HDAC4, a FOXO modulator. Met reduction diminished fecundity and reduced stored lipids, similar to phenotypes obtained via knockdown of the JH biosynthetic enzyme JHAMT and inverse of phenotypes resulting from insulin or JH treatment. These phenotypes suggest that manipulation of JH/IIS pathways can prolong dry periods of the tsetse pregnancy cycle by promoting lipid storage in the fat body.