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

Autores
Garelli, Andres
Año de publicación
2015
Idioma
inglés
Tipo de recurso
documento de conferencia
Estado
versión publicada
Descripción
Developmental stability is the ability of an organism to buffer given traits against environmental and intrinsic perturbations and produce stable genetically determined phenotypes. The processes leading to developmental stability involve physiological, temporal or behavioral adjustments to the developmental program that have been particularly well studied in insects. For instance, if uncoordinated growth occurs in Drosophila imaginal discs, the larval precursors of adult structures, a transient delay in the onset of metamorphosis ensues, allowing extra time for all discs to achieve their specific size. We have recently identified dilp8, a fly specific insulin-like peptide that is produced in damaged imaginal discs and couples tissue growth with developmental timing. Dilp8 transiently delays the onset of metamorphosis by inhibiting the biosynthesis of the molting hormone ecdysone while simultaneously slows down growth of undamaged tissues. Thus, the prolonged larval phase allows tissue regeneration while keeping proportions 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 growth signal remained unknown. We have now found that mutation of Lgr3, a member of the type C1 Leucine-rich repeat-containing G-protein coupled receptors, results in body asymmetries similar to that of dilp8 mutants and the inability to delay development in response to tissue damage. By tagging the endogenous Lgr3 protein with GFP we found that it is expressed and required in a subpopulation of CNS neurons not previously linked to growth control. Our work places Dilp8 and Lgr3 as central players in the interorgan communication system that mediates plasticity to promote developmental stability in Drosophila and reveals a novel neuroendocrine circuit responsive to growth aberrations.
Fil: Garelli, Andres. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Investigaciones Bioquímicas de Bahía Blanca. Universidad Nacional del Sur. Instituto de Investigaciones Bioquímicas de Bahía Blanca; Argentina. Universidad Nacional del Sur; Argentina
Sociedad Argentina de Investigación en Neurociencias XXX Reunión anual
Mar del Plata
Argentina
Sociedad Argentina de Investigación en Neurociencias
Materia
DROSOPHILA
INSULIN LIKE PEPTIDE
DILP8
LGR3
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/230227

id CONICETDig_a17751750afdcf1ff3945df350fb8795
oai_identifier_str oai:ri.conicet.gov.ar:11336/230227
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Dilp8 requires the neuronal relaxin receptor Lgr3 to couple growth to developmental timingGarelli, AndresDROSOPHILAINSULIN LIKE PEPTIDEDILP8LGR3https://purl.org/becyt/ford/1.6https://purl.org/becyt/ford/1Developmental stability is the ability of an organism to buffer given traits against environmental and intrinsic perturbations and produce stable genetically determined phenotypes. The processes leading to developmental stability involve physiological, temporal or behavioral adjustments to the developmental program that have been particularly well studied in insects. For instance, if uncoordinated growth occurs in Drosophila imaginal discs, the larval precursors of adult structures, a transient delay in the onset of metamorphosis ensues, allowing extra time for all discs to achieve their specific size. We have recently identified dilp8, a fly specific insulin-like peptide that is produced in damaged imaginal discs and couples tissue growth with developmental timing. Dilp8 transiently delays the onset of metamorphosis by inhibiting the biosynthesis of the molting hormone ecdysone while simultaneously slows down growth of undamaged tissues. Thus, the prolonged larval phase allows tissue regeneration while keeping proportions 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 growth signal remained unknown. We have now found that mutation of Lgr3, a member of the type C1 Leucine-rich repeat-containing G-protein coupled receptors, results in body asymmetries similar to that of dilp8 mutants and the inability to delay development in response to tissue damage. By tagging the endogenous Lgr3 protein with GFP we found that it is expressed and required in a subpopulation of CNS neurons not previously linked to growth control. Our work places Dilp8 and Lgr3 as central players in the interorgan communication system that mediates plasticity to promote developmental stability in Drosophila and reveals a novel neuroendocrine circuit responsive to growth aberrations.Fil: Garelli, Andres. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Investigaciones Bioquímicas de Bahía Blanca. Universidad Nacional del Sur. Instituto de Investigaciones Bioquímicas de Bahía Blanca; Argentina. Universidad Nacional del Sur; ArgentinaSociedad Argentina de Investigación en Neurociencias XXX Reunión anualMar del PlataArgentinaSociedad Argentina de Investigación en NeurocienciasSociedad Argentina de Investigación en Neurociencias2015info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/conferenceObjectCongresoJournalhttp://purl.org/coar/resource_type/c_5794info:ar-repo/semantics/documentoDeConferenciaapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/230227Dilp8 requires the neuronal relaxin receptor Lgr3 to couple growth to developmental timing; Sociedad Argentina de Investigación en Neurociencias XXX Reunión anual; Mar del Plata; Argentina; 2015; 73-73CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://saneurociencias.org.ar/congresos-san-2/Internacionalinfo:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-29T10:42:35Zoai:ri.conicet.gov.ar:11336/230227instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982025-09-29 10:42:35.855CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Dilp8 requires the neuronal relaxin receptor Lgr3 to couple growth to developmental timing
title Dilp8 requires the neuronal relaxin receptor Lgr3 to couple growth to developmental timing
spellingShingle Dilp8 requires the neuronal relaxin receptor Lgr3 to couple growth to developmental timing
Garelli, Andres
DROSOPHILA
INSULIN LIKE PEPTIDE
DILP8
LGR3
title_short Dilp8 requires the neuronal relaxin receptor Lgr3 to couple growth to developmental timing
title_full Dilp8 requires the neuronal relaxin receptor Lgr3 to couple growth to developmental timing
title_fullStr Dilp8 requires the neuronal relaxin receptor Lgr3 to couple growth to developmental timing
title_full_unstemmed Dilp8 requires the neuronal relaxin receptor Lgr3 to couple growth to developmental timing
title_sort Dilp8 requires the neuronal relaxin receptor Lgr3 to couple growth to developmental timing
dc.creator.none.fl_str_mv Garelli, Andres
author Garelli, Andres
author_facet Garelli, Andres
author_role author
dc.subject.none.fl_str_mv DROSOPHILA
INSULIN LIKE PEPTIDE
DILP8
LGR3
topic DROSOPHILA
INSULIN LIKE PEPTIDE
DILP8
LGR3
purl_subject.fl_str_mv https://purl.org/becyt/ford/1.6
https://purl.org/becyt/ford/1
dc.description.none.fl_txt_mv Developmental stability is the ability of an organism to buffer given traits against environmental and intrinsic perturbations and produce stable genetically determined phenotypes. The processes leading to developmental stability involve physiological, temporal or behavioral adjustments to the developmental program that have been particularly well studied in insects. For instance, if uncoordinated growth occurs in Drosophila imaginal discs, the larval precursors of adult structures, a transient delay in the onset of metamorphosis ensues, allowing extra time for all discs to achieve their specific size. We have recently identified dilp8, a fly specific insulin-like peptide that is produced in damaged imaginal discs and couples tissue growth with developmental timing. Dilp8 transiently delays the onset of metamorphosis by inhibiting the biosynthesis of the molting hormone ecdysone while simultaneously slows down growth of undamaged tissues. Thus, the prolonged larval phase allows tissue regeneration while keeping proportions 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 growth signal remained unknown. We have now found that mutation of Lgr3, a member of the type C1 Leucine-rich repeat-containing G-protein coupled receptors, results in body asymmetries similar to that of dilp8 mutants and the inability to delay development in response to tissue damage. By tagging the endogenous Lgr3 protein with GFP we found that it is expressed and required in a subpopulation of CNS neurons not previously linked to growth control. Our work places Dilp8 and Lgr3 as central players in the interorgan communication system that mediates plasticity to promote developmental stability in Drosophila and reveals a novel neuroendocrine circuit responsive to growth aberrations.
Fil: Garelli, Andres. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Investigaciones Bioquímicas de Bahía Blanca. Universidad Nacional del Sur. Instituto de Investigaciones Bioquímicas de Bahía Blanca; Argentina. Universidad Nacional del Sur; Argentina
Sociedad Argentina de Investigación en Neurociencias XXX Reunión anual
Mar del Plata
Argentina
Sociedad Argentina de Investigación en Neurociencias
description Developmental stability is the ability of an organism to buffer given traits against environmental and intrinsic perturbations and produce stable genetically determined phenotypes. The processes leading to developmental stability involve physiological, temporal or behavioral adjustments to the developmental program that have been particularly well studied in insects. For instance, if uncoordinated growth occurs in Drosophila imaginal discs, the larval precursors of adult structures, a transient delay in the onset of metamorphosis ensues, allowing extra time for all discs to achieve their specific size. We have recently identified dilp8, a fly specific insulin-like peptide that is produced in damaged imaginal discs and couples tissue growth with developmental timing. Dilp8 transiently delays the onset of metamorphosis by inhibiting the biosynthesis of the molting hormone ecdysone while simultaneously slows down growth of undamaged tissues. Thus, the prolonged larval phase allows tissue regeneration while keeping proportions 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 growth signal remained unknown. We have now found that mutation of Lgr3, a member of the type C1 Leucine-rich repeat-containing G-protein coupled receptors, results in body asymmetries similar to that of dilp8 mutants and the inability to delay development in response to tissue damage. By tagging the endogenous Lgr3 protein with GFP we found that it is expressed and required in a subpopulation of CNS neurons not previously linked to growth control. Our work places Dilp8 and Lgr3 as central players in the interorgan communication system that mediates plasticity to promote developmental stability in Drosophila and reveals a novel neuroendocrine circuit responsive to growth aberrations.
publishDate 2015
dc.date.none.fl_str_mv 2015
dc.type.none.fl_str_mv info:eu-repo/semantics/publishedVersion
info:eu-repo/semantics/conferenceObject
Congreso
Journal
http://purl.org/coar/resource_type/c_5794
info:ar-repo/semantics/documentoDeConferencia
status_str publishedVersion
format conferenceObject
dc.identifier.none.fl_str_mv http://hdl.handle.net/11336/230227
Dilp8 requires the neuronal relaxin receptor Lgr3 to couple growth to developmental timing; Sociedad Argentina de Investigación en Neurociencias XXX Reunión anual; Mar del Plata; Argentina; 2015; 73-73
CONICET Digital
CONICET
url http://hdl.handle.net/11336/230227
identifier_str_mv Dilp8 requires the neuronal relaxin receptor Lgr3 to couple growth to developmental timing; Sociedad Argentina de Investigación en Neurociencias XXX Reunión anual; Mar del Plata; Argentina; 2015; 73-73
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/url/https://saneurociencias.org.ar/congresos-san-2/
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/pdf
application/pdf
dc.coverage.none.fl_str_mv Internacional
dc.publisher.none.fl_str_mv Sociedad Argentina de Investigación en Neurociencias
publisher.none.fl_str_mv Sociedad Argentina de Investigación en Neurociencias
dc.source.none.fl_str_mv reponame:CONICET Digital (CONICET)
instname:Consejo Nacional de Investigaciones Científicas y Técnicas
reponame_str CONICET Digital (CONICET)
collection CONICET Digital (CONICET)
instname_str Consejo Nacional de Investigaciones Científicas y Técnicas
repository.name.fl_str_mv CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas
repository.mail.fl_str_mv dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar
_version_ 1844614458747387904
score 13.070432