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

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