Neuroendocrine control of puparium morphogenesis

GARELLI ANDRÉS; JOANA PEREIRINHA; PRADO SPALM FACUNDO; CASIMIRO ANDREIA; MACEDO ANDRE; VOLONTÉ YANEL ANDREA; HEREDIA FABIANA; GONTIJO ALISSON

Tochigi

Workshop; The 3rd International Insect Hormone (21st Ecdysone) Workshop; 2017

Drosophila larvae undergo a dramatic change in body shape at the end of the larval growthperiod when the long, thin, flexible and transparent cuticle of the larvae is transformed into thepuparium. This remodeling is achieved by a series of muscular contractions such as retraction ofthe anterior segments and body contraction, and accompanied by structural remodeling of thecuticle that include cuticular hardening and tanning. Even though the onset of the metamorphosisprogram is known to be under the control of ecdysone, other molecular players have been shownor hypothesized to act downstream of it to mediate different aspects of these behavioral andmorphogenetic processes. Serendipitously, we observed that animals lacking the relaxin-receptorlike G-protein coupled receptor (GPCR) Lgr3 produce a thin and elongated puparium, indicating thatLgr3 is required for proper puparium morphogenesis. We will present evidence that this activity isseparable from the previously described role for Lgr3 during larval development, where it has beenshown to act in a subpopulation of CNS neurons to coordinate by inhibiting ecdysone biosynthesis,in a Drosophila insulin-like peptide 8 (Dilp8)-dependent fashion. Rather, our results are consistentwith Lgr3 acting in a distinct population of neurons that respond to a developmentally-triggeredsurge of carcass-derived Dilp8 peptide that occurs at the onset of pupariation. Hence, the peptidehormone Dilp8 and the GPCR Lgr3 constitute a new neuroendocrine pathway directly contributingto puparium morphogenesis.