Neural modulation of systemic stress response requires the insulin like-peptide INS-3 in C. elegans

Autores
Veuthey, Tania Vanesa; Giunti, Sebastián; de Rosa, Maria Jose; Rayes, Diego Hernán
Año de publicación
2019
Idioma
inglés
Tipo de recurso
documento de conferencia
Estado
versión publicada
Descripción
Perpetuation of the flight response inhibits defensive cytoprotective mechanisms, leading to early onset of age-related disorders from invertebrates to mammals. We have recently shown that, in C. elegans, the flight response induces neuronal release of Tyramine (TA, invertebrate analog of adrenaline), that stimulates the adrenergic-like receptor TYRA-3 in the intestine. This leads to the activation of the DAF-2/Insulin/IGF-1 pathway in non-intestinal cells and the inhibition of cytoprotective mechanisms. However, the signals that link the activation of TYRA-3 in the intestine with the DAF-2 insulin receptor in other tissues is unknown. We, therefore, performed a screening of Insulin like-peptides expressed in the intestine by RNAi and identified that lack of ins-3 improves resistance to oxidative and thermal stress. This resistant phenotype cannot be reversed by exogenous TA and it is mediated, at least partially, by DAF-16/FOXO. Moreover, by using genetics we found that tyra-3 and ins-3 act in the same pathway. In addition, we found that only the intestinal rescue of ins-3 null mutants was able to restore the resistance to wild-type levels. We propose that INS-3 could be the signal molecule that connects the intestine, where TA receptor is expressed, with distal tissues. Given the high degree of conservation of fundamental mechanisms, this work can contribute to the understanding of neurohormonal coordination of stress responses in animals.
Fil: Veuthey, Tania Vanesa. 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. Departamento de Biología, Bioquímica y Farmacia; Argentina
Fil: Giunti, Sebastián. 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. Departamento de Biología, Bioquímica y Farmacia; Argentina
Fil: de Rosa, Maria Jose. 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. Departamento de Biología, Bioquímica y Farmacia; Argentina
Fil: Rayes, Diego Hernán. 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. Departamento de Biología, Bioquímica y Farmacia; Argentina
XXXIV Reunión Anual de la Sociedad Argentina de Investigación en Neurociencias
Villa Carlos Paz
Argentina
Sociedad Argentina de Investigación en Neurociencias
Materia
c elegans
Insulin
stress
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:11336/192510

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network_name_str CONICET Digital (CONICET)
spelling Neural modulation of systemic stress response requires the insulin like-peptide INS-3 in C. elegansVeuthey, Tania VanesaGiunti, Sebastiánde Rosa, Maria JoseRayes, Diego Hernánc elegansInsulinstresshttps://purl.org/becyt/ford/1.7https://purl.org/becyt/ford/1Perpetuation of the flight response inhibits defensive cytoprotective mechanisms, leading to early onset of age-related disorders from invertebrates to mammals. We have recently shown that, in C. elegans, the flight response induces neuronal release of Tyramine (TA, invertebrate analog of adrenaline), that stimulates the adrenergic-like receptor TYRA-3 in the intestine. This leads to the activation of the DAF-2/Insulin/IGF-1 pathway in non-intestinal cells and the inhibition of cytoprotective mechanisms. However, the signals that link the activation of TYRA-3 in the intestine with the DAF-2 insulin receptor in other tissues is unknown. We, therefore, performed a screening of Insulin like-peptides expressed in the intestine by RNAi and identified that lack of ins-3 improves resistance to oxidative and thermal stress. This resistant phenotype cannot be reversed by exogenous TA and it is mediated, at least partially, by DAF-16/FOXO. Moreover, by using genetics we found that tyra-3 and ins-3 act in the same pathway. In addition, we found that only the intestinal rescue of ins-3 null mutants was able to restore the resistance to wild-type levels. We propose that INS-3 could be the signal molecule that connects the intestine, where TA receptor is expressed, with distal tissues. Given the high degree of conservation of fundamental mechanisms, this work can contribute to the understanding of neurohormonal coordination of stress responses in animals.Fil: Veuthey, Tania Vanesa. 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. Departamento de Biología, Bioquímica y Farmacia; ArgentinaFil: Giunti, Sebastián. 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. Departamento de Biología, Bioquímica y Farmacia; ArgentinaFil: de Rosa, Maria Jose. 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. Departamento de Biología, Bioquímica y Farmacia; ArgentinaFil: Rayes, Diego Hernán. 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. Departamento de Biología, Bioquímica y Farmacia; ArgentinaXXXIV Reunión Anual de la Sociedad Argentina de Investigación en NeurocienciasVilla Carlos PazArgentinaSociedad Argentina de Investigación en NeurocienciasSociedad Argentina de Investigación en Neurociencias2019info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/conferenceObjectCongresoBookhttp://purl.org/coar/resource_type/c_5794info:ar-repo/semantics/documentoDeConferenciaapplication/pdfapplication/pdfapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/192510Neural modulation of systemic stress response requires the insulin like-peptide INS-3 in C. elegans; XXXIV Reunión Anual de la Sociedad Argentina de Investigación en Neurociencias; Villa Carlos Paz; Argentina; 2019; 150-150CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://saneurociencias.org.ar/Nacionalinfo:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-10-15T15:09:39Zoai:ri.conicet.gov.ar:11336/192510instacron: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:34982025-10-15 15:09:39.765CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Neural modulation of systemic stress response requires the insulin like-peptide INS-3 in C. elegans
title Neural modulation of systemic stress response requires the insulin like-peptide INS-3 in C. elegans
spellingShingle Neural modulation of systemic stress response requires the insulin like-peptide INS-3 in C. elegans
Veuthey, Tania Vanesa
c elegans
Insulin
stress
title_short Neural modulation of systemic stress response requires the insulin like-peptide INS-3 in C. elegans
title_full Neural modulation of systemic stress response requires the insulin like-peptide INS-3 in C. elegans
title_fullStr Neural modulation of systemic stress response requires the insulin like-peptide INS-3 in C. elegans
title_full_unstemmed Neural modulation of systemic stress response requires the insulin like-peptide INS-3 in C. elegans
title_sort Neural modulation of systemic stress response requires the insulin like-peptide INS-3 in C. elegans
dc.creator.none.fl_str_mv Veuthey, Tania Vanesa
Giunti, Sebastián
de Rosa, Maria Jose
Rayes, Diego Hernán
author Veuthey, Tania Vanesa
author_facet Veuthey, Tania Vanesa
Giunti, Sebastián
de Rosa, Maria Jose
Rayes, Diego Hernán
author_role author
author2 Giunti, Sebastián
de Rosa, Maria Jose
Rayes, Diego Hernán
author2_role author
author
author
dc.subject.none.fl_str_mv c elegans
Insulin
stress
topic c elegans
Insulin
stress
purl_subject.fl_str_mv https://purl.org/becyt/ford/1.7
https://purl.org/becyt/ford/1
dc.description.none.fl_txt_mv Perpetuation of the flight response inhibits defensive cytoprotective mechanisms, leading to early onset of age-related disorders from invertebrates to mammals. We have recently shown that, in C. elegans, the flight response induces neuronal release of Tyramine (TA, invertebrate analog of adrenaline), that stimulates the adrenergic-like receptor TYRA-3 in the intestine. This leads to the activation of the DAF-2/Insulin/IGF-1 pathway in non-intestinal cells and the inhibition of cytoprotective mechanisms. However, the signals that link the activation of TYRA-3 in the intestine with the DAF-2 insulin receptor in other tissues is unknown. We, therefore, performed a screening of Insulin like-peptides expressed in the intestine by RNAi and identified that lack of ins-3 improves resistance to oxidative and thermal stress. This resistant phenotype cannot be reversed by exogenous TA and it is mediated, at least partially, by DAF-16/FOXO. Moreover, by using genetics we found that tyra-3 and ins-3 act in the same pathway. In addition, we found that only the intestinal rescue of ins-3 null mutants was able to restore the resistance to wild-type levels. We propose that INS-3 could be the signal molecule that connects the intestine, where TA receptor is expressed, with distal tissues. Given the high degree of conservation of fundamental mechanisms, this work can contribute to the understanding of neurohormonal coordination of stress responses in animals.
Fil: Veuthey, Tania Vanesa. 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. Departamento de Biología, Bioquímica y Farmacia; Argentina
Fil: Giunti, Sebastián. 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. Departamento de Biología, Bioquímica y Farmacia; Argentina
Fil: de Rosa, Maria Jose. 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. Departamento de Biología, Bioquímica y Farmacia; Argentina
Fil: Rayes, Diego Hernán. 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. Departamento de Biología, Bioquímica y Farmacia; Argentina
XXXIV Reunión Anual de la Sociedad Argentina de Investigación en Neurociencias
Villa Carlos Paz
Argentina
Sociedad Argentina de Investigación en Neurociencias
description Perpetuation of the flight response inhibits defensive cytoprotective mechanisms, leading to early onset of age-related disorders from invertebrates to mammals. We have recently shown that, in C. elegans, the flight response induces neuronal release of Tyramine (TA, invertebrate analog of adrenaline), that stimulates the adrenergic-like receptor TYRA-3 in the intestine. This leads to the activation of the DAF-2/Insulin/IGF-1 pathway in non-intestinal cells and the inhibition of cytoprotective mechanisms. However, the signals that link the activation of TYRA-3 in the intestine with the DAF-2 insulin receptor in other tissues is unknown. We, therefore, performed a screening of Insulin like-peptides expressed in the intestine by RNAi and identified that lack of ins-3 improves resistance to oxidative and thermal stress. This resistant phenotype cannot be reversed by exogenous TA and it is mediated, at least partially, by DAF-16/FOXO. Moreover, by using genetics we found that tyra-3 and ins-3 act in the same pathway. In addition, we found that only the intestinal rescue of ins-3 null mutants was able to restore the resistance to wild-type levels. We propose that INS-3 could be the signal molecule that connects the intestine, where TA receptor is expressed, with distal tissues. Given the high degree of conservation of fundamental mechanisms, this work can contribute to the understanding of neurohormonal coordination of stress responses in animals.
publishDate 2019
dc.date.none.fl_str_mv 2019
dc.type.none.fl_str_mv info:eu-repo/semantics/publishedVersion
info:eu-repo/semantics/conferenceObject
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Book
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/11336/192510
Neural modulation of systemic stress response requires the insulin like-peptide INS-3 in C. elegans; XXXIV Reunión Anual de la Sociedad Argentina de Investigación en Neurociencias; Villa Carlos Paz; Argentina; 2019; 150-150
CONICET Digital
CONICET
url http://hdl.handle.net/11336/192510
identifier_str_mv Neural modulation of systemic stress response requires the insulin like-peptide INS-3 in C. elegans; XXXIV Reunión Anual de la Sociedad Argentina de Investigación en Neurociencias; Villa Carlos Paz; Argentina; 2019; 150-150
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
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https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
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dc.publisher.none.fl_str_mv Sociedad Argentina de Investigación en Neurociencias
publisher.none.fl_str_mv Sociedad Argentina de Investigación en Neurociencias
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