Neuroendocrine control of morphogenesis

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

Tomar

Encuentro; DrosTuga: 2017 Annual Portuguese Drosophila Meeting; 2017

Drosophila larvae undergo a dramatic change in body shape at the end of the larval growthperiod: the long, transparent, and flexible larval cuticle is remodeled into the short, tanned, andrigid puparium, the skin inside which higher dipteran larvae undergo metamorphosis. This bodychange is achieved by a series of stereotyped muscular contractions accompanied by structuralsclerotization of the cuticle. While the onset of the whole metamorphosis program is known tobe under the control of the hormone ecdysone, the molecular pathways mediating thedownstream behavioral and morphogenetic processes are less understood. Serendipitously, weobserved that larvae lacking the conserved relaxin-receptor like G-protein coupled receptor(GPCR), Lgr3, fail to shorten into the characteristic puparium form, so that their cuticlesclerotizes into an elongated larva-like puparium instead. Tissue and cell-type-specific RNAiexperiments revealed that this Lgr3 activity is separable from its previously described role duringlarval development, where it has been shown to act in a subpopulation of CNS neurons tocoordinate imaginal disc growth with developmental timing, in a Drosophila insulin-like peptide8 (Dilp8)-dependent manner. Rather, our results indicate that Lgr3 acts in a distinct populationof CNS neurons that respond to a strong developmentally-triggered pulse of carcass-derivedDilp8 peptide, which occurs within a 30-60-min window at the onset of pupariation. Hence, thepeptide hormone Dilp8 and the neuronal GPCR Lgr3 constitute a new interorgan communicationpathway controlling puparium morphogenesis.