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
- Institución
- Consejo Nacional de Investigaciones Científicas y Técnicas
- OAI Identificador
- oai:ri.conicet.gov.ar:11336/192510
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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 Congreso 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 |
dc.relation.none.fl_str_mv |
info:eu-repo/semantics/altIdentifier/url/https://saneurociencias.org.ar/ |
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info:eu-repo/semantics/openAccess https://creativecommons.org/licenses/by-nc-sa/2.5/ar/ |
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openAccess |
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https://creativecommons.org/licenses/by-nc-sa/2.5/ar/ |
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application/pdf application/pdf application/pdf application/pdf application/pdf |
dc.coverage.none.fl_str_mv |
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Sociedad Argentina de Investigación en Neurociencias |
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Sociedad Argentina de Investigación en Neurociencias |
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