The relaxin receptor Lgr3 mediates growth coordination and developmental delay during Drosophila melanogaster imaginal disc regeneration

摘要: Damage to Drosophila melanogaster imaginal discs activates a regeneration checkpoint that 1) extends larval development and 2) coordinates the of damaged disc with growth undamaged discs. These two systemic responses damage are both mediated by Dilp8, member insulin/IGF/relaxin family peptide hormones, which is released regenerating Growth coordination between dependent on Dilp8 activation NOS in prothoracic gland (PG), slows limiting ecdysone synthesis. Here we demonstrate relaxin receptor homologue Lgr3, leucine-rich repeat-containing G-protein coupled receptor, required for Dilp8-dependent developmental delay during checkpoint. Lgr3 regulates these via distinct mechanisms different tissues. Using tissue-specific RNAi disruption expression, show functions PG upstream nitric oxide synthase (NOS), necessary When depleted from neurons, no longer produces either or inhibition. To reconcile discrete tissue requirements regenerative coordination, activity CNS following damage. Together, results identify new roles mediating signaling regulate timing.