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

ANDRES GARELLI,

Mar del Plata

Congreso; XXX SAN Annual Meeting; 2015

Sociedad Argentina de Investigación en Neurociencias

Developmental stability is the ability of an organism to buffer given traitsagainst environmental and intrinsic perturbations and produce stablegenetically determined phenotypes. The processes leading to developmentalstability involve physiological, temporal or behavioral adjustments to thedevelopmental program that have been particularly well studied in insects. Forinstance, if uncoordinated growth occurs in Drosophila imaginal discs, thelarval precursors of adult structures, a transient delay in the onset ofmetamorphosis ensues, allowing extra time for all discs to achieve theirspecific size. We have recently identified dilp8, a fly specific insulin-likepeptide that is produced in damaged imaginal discs and couples tissue growthwith developmental timing. Dilp8 transiently delays the onset ofmetamorphosis by inhibiting the biosynthesis of the molting hormoneecdysone while simultaneously slows down growth of undamaged tissues.Thus, the prolonged larval phase allows tissue regeneration while keepingproportions with unaffected discs and results in proportionate adults.Accordingly, loss of dilp8 increases intra-individual asymmetry(1). However,which molecules and tissues sense and/or transmit this abnormal growthsignal remained unknown. We have now found that mutation of Lgr3, amember of the type C1 Leucine-rich repeat-containing G-protein coupledreceptors, results in body asymmetries similar to that of dilp8 mutants and theinability to delay development in response to tissue damage. By tagging theendogenous Lgr3 protein with GFP we found that it is expressed and requiredin a subpopulation of CNS neurons not previously linked to growth control.Our work places Dilp8 and Lgr3 as central players in the interorgancommunication system that mediates plasticity to promote developmentalstability in Drosophila and reveals a novel neuroendocrine circuit responsive togrowth aberrations.