The Insulin and Tor signaling pathways directly regulate cuticle melanization in Drosophila. Jennifer A. Kennell, Iryna Shakhmantsir. Biology, Vassar College, Poughkeepsie, NY.

   In addition to its mechanical properties, the pigmented cuticle of insects can play a role in thermoregulation, desiccation tolerance, mimicry and sexual selection. Cuticle pigmentation is a phenotypically plastic trait, with environmental factors such as temperature and nutrition influencing the extent of melanization in Drosophila. We present evidence suggesting a novel role for the nutrient sensing Insulin and Target of Rapamycin (Tor) pathways in directly regulating pigmentation of adult cuticle in Drosophila melanogaster. We found that activation of Insulin/PI3K signaling along the dorsal midline using the pnr-Gal4 driver results in a cell autonomous increase in melanization of the adult cuticle. Conversely, inhibition of the pathway causes decreased pigmentation of both the abdomen and thorax. Insulin/PI3K signaling likely promotes pigmentation in part through inhibition of dFOXO. Given that the Insulin/PI3K pathway interacts with the Tor pathway, we also tested the ability of Tor signaling to regulate pigmentation. We found that activation of the Tor pathway causes increased pigmentation, as does activation of S6K, an effector of the Tor pathway. Interestingly, modulation of these pathways using the pnr-Gal4 driver could change pigmentation without altering other aspects of cuticle development such as segment and bristle formation, suggesting this effect on pigmentation is specific and not due to the indirect effects of altered cell migration, division or differentiation. Previous studies in Drosophila and other insects have found a positive association between nutrient status and melanization. Some have proposed that this connection between nutrition and pigmentation may be due to changes in availability of substrates for melanin production, such as tyrosine. Our data suggests that nutritional control of cuticular melanization in Drosophila melanogaster may be mediated by the Insulin and Tor signaling pathways.