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

Andres Garelli (), Fabiana Heredia, Andreia P. Casimiro, Andre Macedo, Catarina Nunes, Marcia Garcez, Angela R. Mantas Dias, Yanel A. Volonte, Thomas Uhlmann, Esther Caparros, Takashi Koyama and Alisson M. Gontijo ()
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Andres Garelli: Integrative Biomedicine Laboratory, CEDOC—Chronic Diseases Research Center, NOVA Medical School | Faculdade de Ciencias Medicas, NOVA University of Lisbon
Fabiana Heredia: Integrative Biomedicine Laboratory, CEDOC—Chronic Diseases Research Center, NOVA Medical School | Faculdade de Ciencias Medicas, NOVA University of Lisbon
Andreia P. Casimiro: Integrative Biomedicine Laboratory, CEDOC—Chronic Diseases Research Center, NOVA Medical School | Faculdade de Ciencias Medicas, NOVA University of Lisbon
Andre Macedo: Integrative Biomedicine Laboratory, CEDOC—Chronic Diseases Research Center, NOVA Medical School | Faculdade de Ciencias Medicas, NOVA University of Lisbon
Catarina Nunes: Integrative Biomedicine Laboratory, CEDOC—Chronic Diseases Research Center, NOVA Medical School | Faculdade de Ciencias Medicas, NOVA University of Lisbon
Marcia Garcez: Integrative Biomedicine Laboratory, CEDOC—Chronic Diseases Research Center, NOVA Medical School | Faculdade de Ciencias Medicas, NOVA University of Lisbon
Angela R. Mantas Dias: Integrative Biomedicine Laboratory, CEDOC—Chronic Diseases Research Center, NOVA Medical School | Faculdade de Ciencias Medicas, NOVA University of Lisbon
Yanel A. Volonte: Instituto de Investigaciones Bioquímicas de Bahía Blanca (INIBIBB), CONICET and Universidad Nacional del Sur
Thomas Uhlmann: Dualsystems Biotech AG
Esther Caparros: Facultad de Medicina, Universidad Miguel Hernández
Takashi Koyama: Development, Evolution and the Environment Laboratory, Instituto Gulbenkian de Ciência
Alisson M. Gontijo: Integrative Biomedicine Laboratory, CEDOC—Chronic Diseases Research Center, NOVA Medical School | Faculdade de Ciencias Medicas, NOVA University of Lisbon

Nature Communications, 2015, vol. 6, issue 1, 1-14

Abstract: Abstract How different organs in the body sense growth perturbations in distant tissues to coordinate their size during development is poorly understood. Here we mutate an invertebrate orphan relaxin 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 RNA intereference (RNAi) against Lgr3 suppresses the delay in pupariation induced by imaginal disc growth perturbation or ectopic Dilp8 expression. By tagging endogenous Lgr3 and performing 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 respond specifically to ectopic Dilp8 by increasing cAMP-dependent signalling. Our work sheds new light on the function and evolution of relaxin receptors and reveals a novel neuroendocrine circuit responsive to growth aberrations.

Date: 2015
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DOI: 10.1038/ncomms9732

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