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
- Institución
- Consejo Nacional de Investigaciones Científicas y Técnicas
- OAI Identificador
- oai:ri.conicet.gov.ar:11336/230227
Ver los metadatos del registro completo
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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 |
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1844614458747387904 |
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13.070432 |