Dilp8 requires the neuronal relaxin receptor Lgr3 to couple growth to developmental timing

GARELLI ANDRÉS; HEREDIA FABIANA; CASIMIRO ANDREIA; MACEDO ANDRE; NUNES CATARINA; GARCEZ MARCIA; MANTAS DIAS ANGELA; VOLONTÉ YANEL ANDREA; UHLMANN THOMAS; CAPARROS ESTHER; KOYAMA TAKASHI; GONTIJO ALISSON

NATURE COMMUNICATIONS

Macmillan Publishers

Año: 2015 vol. 6 p. 1 - 14

2041-1723

How different organs in the body sense growth perturbations in distant tissues to coordinatetheir size during development is poorly understood. Here we mutate an invertebrate orphanrelaxin receptor gene, the Drosophila Leucine-rich repeat-containing G protein-coupled receptor 3(Lgr3), and find body asymmetries similar to those found in insulin-like peptide 8 (dilp8)mutants, which fail to coordinate growth with developmental timing. Indeed, mutation or RNAintereference (RNAi) against Lgr3 suppresses the delay in pupariation induced by imaginaldisc growth perturbation or ectopic Dilp8 expression. By tagging endogenous Lgr3 andperforming cell type-specific RNAi, we map this Lgr3 activity to a new subset of CNS neurons,four of which are a pair of bilateral pars intercerebralis Lgr3-positive (PIL) neurons that respondspecifically to ectopic Dilp8 by increasing cAMP-dependent signalling. Our work sheds newlight on the function and evolution of relaxin receptors and reveals a novel neuroendocrinecircuit responsive to growth aberrations.