774B Poster - 12. Physiology, metabolism and aging
Friday April 08, 2:00 PM - 4:00 PM

Authors:
Samuel Goldsmith; Stuart Newfeld

Affiliation: School of Life Sciences, Arizona State University, Tempe AZ

Keywords:
l. Insulin signaling/ insulin-like peptides; i. hormones

Previous studies in our lab of dILP2 in the adult female brain showed that dCORL (fuss in Flybase) was required for dILP2 expression in a subset of insulin producing cells (IPCs). To test the hypothesis that dCORL is acting downstream of dSmad2[SG(1] in IPCs, as was shown earlier in the mushroom body of third instar larvae, we generated dSmad2 mutant MARCM clones in IPCs. Additionally, a series of follow-up experiments in IPCs were completed and the results were consistent with the data from the dSmad2 mutant MARCM clones. Employing a dCORL.Gal4 driver expressed in IPCs, dSmad2 mutant MARCM clones displayed excess dILP2 expression in comparison to adjacent wild type siblings (n=5; p=0.057). The overexpression phenotype was also seen with dSmad2 RNAi in IPCs driven by dCORL.Gal4 (n=14; p=0.013). The overexpression phenotype was rescued when expressing UAS.dSmad2 in mutant MARCM clones (n=7; p=0.67). The dSmad2 mutant phenotype appears similar to dILP2 overexpression in mutants for unpaired-2 that prevent dILP2 secretion. Studies with TrpA1 to test the secretion hypothesis are in progress. Overall, our study shows that dCORL functions independently of dSmad2 in the regulation of dILP2 expression in adult IPCs.