Neural modulation of systemic stress response requires the insulin like-peptide INS-3
- Autores
- Veuthey, Tania Vanesa; Giunti, Sebastián; de Rosa, Maria Jos; Alkema, Mark; Rayes, Diego Hernán
- Año de publicación
- 2023
- Idioma
- inglés
- Tipo de recurso
- documento de conferencia
- Estado
- versión publicada
- Descripción
- Throughout the animal kingdom, the perpetuation of the flight response leads to reduced ability to cope with environmental challenges, a drastic lifespan reduction, and an increase in disease susceptibility. We showed that, in C. elegans, the tyraminergic neuron RIM supplies a state- dependent neural switch between acute flight and long-term environmental stress responses. During the flight-stress response RIM neurons release TA, which stimulates the intestinal adrenergic-like receptor TYRA-3. This leads to DAF-2/Insulin/IGF- 1 pathway activation and inhibition of cytoprotective mechanisms in the intestine and other tissues. We hypothesized that TYRA-3 stimulates the release of Insulin-Like Peptides (ILPs) from the intestine that can systemically activate the DAF-2 insulin/ IGF1 receptors. We focused on strong agonist ILPs that are expressed in the intestine (INS-3, -4, -6, -32, and DAF-28). We found that ins-3 mutants are resistant to both heat and oxidative stress, much like tyra-3 mutants. Moreover, ins-3 mutants are resistant to the impairment of stress resistance upon exposure to exogenous tyramine. In addition, ins-3;tyra-3 double mutants are as resistant to environmental stress as single mutants, suggesting that both genes act in the same pathway. Since ins-3 is expressed in neurons and the intestine, we performed tissue-specific rescue experiments. We found that expression of ins-3 in the intestine restores stress resistance to wild-type levels. Taken together, our results suggest that intestinal activation of TYRA-3 by the escape neurohormone TA leads to INS-3 release which acts as an endocrine, autocrine, and/or paracrine signal to activate DAF-2 in different tissues.
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
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
Fil: de Rosa, Maria Jos. 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
Fil: Alkema, Mark. University Of Massachussets. Medical School. School Of Medicine; Estados Unidos
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
Third Latin American Worm Meeting
Valparaiso
Chile
Centro Interdisciplinario de Neurociencia Valparaíso - Materia
-
C. ELEGANS
STRESS RESPONSE
INSULINE
NEURONAL MODULATION - 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:11336/250662
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Neural modulation of systemic stress response requires the insulin like-peptide INS-3Veuthey, Tania VanesaGiunti, Sebastiánde Rosa, Maria JosAlkema, MarkRayes, Diego HernánC. ELEGANSSTRESS RESPONSEINSULINENEURONAL MODULATIONhttps://purl.org/becyt/ford/1.7https://purl.org/becyt/ford/1Throughout the animal kingdom, the perpetuation of the flight response leads to reduced ability to cope with environmental challenges, a drastic lifespan reduction, and an increase in disease susceptibility. We showed that, in C. elegans, the tyraminergic neuron RIM supplies a state- dependent neural switch between acute flight and long-term environmental stress responses. During the flight-stress response RIM neurons release TA, which stimulates the intestinal adrenergic-like receptor TYRA-3. This leads to DAF-2/Insulin/IGF- 1 pathway activation and inhibition of cytoprotective mechanisms in the intestine and other tissues. We hypothesized that TYRA-3 stimulates the release of Insulin-Like Peptides (ILPs) from the intestine that can systemically activate the DAF-2 insulin/ IGF1 receptors. We focused on strong agonist ILPs that are expressed in the intestine (INS-3, -4, -6, -32, and DAF-28). We found that ins-3 mutants are resistant to both heat and oxidative stress, much like tyra-3 mutants. Moreover, ins-3 mutants are resistant to the impairment of stress resistance upon exposure to exogenous tyramine. In addition, ins-3;tyra-3 double mutants are as resistant to environmental stress as single mutants, suggesting that both genes act in the same pathway. Since ins-3 is expressed in neurons and the intestine, we performed tissue-specific rescue experiments. We found that expression of ins-3 in the intestine restores stress resistance to wild-type levels. Taken together, our results suggest that intestinal activation of TYRA-3 by the escape neurohormone TA leads to INS-3 release which acts as an endocrine, autocrine, and/or paracrine signal to activate DAF-2 in different tissues.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; 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; ArgentinaFil: de Rosa, Maria Jos. 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; ArgentinaFil: Alkema, Mark. University Of Massachussets. Medical School. School Of Medicine; Estados UnidosFil: 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; ArgentinaThird Latin American Worm MeetingValparaisoChileCentro Interdisciplinario de Neurociencia ValparaísoLatin American worm meeting2023info: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/11336/250662Neural modulation of systemic stress response requires the insulin like-peptide INS-3; Third Latin American Worm Meeting; Valparaiso; Chile; 2023; 42-42CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://cinv.uv.cl/en/3rd-la-worm-meeting/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 Técnicas2025-09-29T09:35:59Zoai:ri.conicet.gov.ar:11336/250662instacron: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 09:35:59.479CONICET 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 |
title |
Neural modulation of systemic stress response requires the insulin like-peptide INS-3 |
spellingShingle |
Neural modulation of systemic stress response requires the insulin like-peptide INS-3 Veuthey, Tania Vanesa C. ELEGANS STRESS RESPONSE INSULINE NEURONAL MODULATION |
title_short |
Neural modulation of systemic stress response requires the insulin like-peptide INS-3 |
title_full |
Neural modulation of systemic stress response requires the insulin like-peptide INS-3 |
title_fullStr |
Neural modulation of systemic stress response requires the insulin like-peptide INS-3 |
title_full_unstemmed |
Neural modulation of systemic stress response requires the insulin like-peptide INS-3 |
title_sort |
Neural modulation of systemic stress response requires the insulin like-peptide INS-3 |
dc.creator.none.fl_str_mv |
Veuthey, Tania Vanesa Giunti, Sebastián de Rosa, Maria Jos Alkema, Mark Rayes, Diego Hernán |
author |
Veuthey, Tania Vanesa |
author_facet |
Veuthey, Tania Vanesa Giunti, Sebastián de Rosa, Maria Jos Alkema, Mark Rayes, Diego Hernán |
author_role |
author |
author2 |
Giunti, Sebastián de Rosa, Maria Jos Alkema, Mark Rayes, Diego Hernán |
author2_role |
author author author author |
dc.subject.none.fl_str_mv |
C. ELEGANS STRESS RESPONSE INSULINE NEURONAL MODULATION |
topic |
C. ELEGANS STRESS RESPONSE INSULINE NEURONAL MODULATION |
purl_subject.fl_str_mv |
https://purl.org/becyt/ford/1.7 https://purl.org/becyt/ford/1 |
dc.description.none.fl_txt_mv |
Throughout the animal kingdom, the perpetuation of the flight response leads to reduced ability to cope with environmental challenges, a drastic lifespan reduction, and an increase in disease susceptibility. We showed that, in C. elegans, the tyraminergic neuron RIM supplies a state- dependent neural switch between acute flight and long-term environmental stress responses. During the flight-stress response RIM neurons release TA, which stimulates the intestinal adrenergic-like receptor TYRA-3. This leads to DAF-2/Insulin/IGF- 1 pathway activation and inhibition of cytoprotective mechanisms in the intestine and other tissues. We hypothesized that TYRA-3 stimulates the release of Insulin-Like Peptides (ILPs) from the intestine that can systemically activate the DAF-2 insulin/ IGF1 receptors. We focused on strong agonist ILPs that are expressed in the intestine (INS-3, -4, -6, -32, and DAF-28). We found that ins-3 mutants are resistant to both heat and oxidative stress, much like tyra-3 mutants. Moreover, ins-3 mutants are resistant to the impairment of stress resistance upon exposure to exogenous tyramine. In addition, ins-3;tyra-3 double mutants are as resistant to environmental stress as single mutants, suggesting that both genes act in the same pathway. Since ins-3 is expressed in neurons and the intestine, we performed tissue-specific rescue experiments. We found that expression of ins-3 in the intestine restores stress resistance to wild-type levels. Taken together, our results suggest that intestinal activation of TYRA-3 by the escape neurohormone TA leads to INS-3 release which acts as an endocrine, autocrine, and/or paracrine signal to activate DAF-2 in different tissues. 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 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 Fil: de Rosa, Maria Jos. 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 Fil: Alkema, Mark. University Of Massachussets. Medical School. School Of Medicine; Estados Unidos 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 Third Latin American Worm Meeting Valparaiso Chile Centro Interdisciplinario de Neurociencia Valparaíso |
description |
Throughout the animal kingdom, the perpetuation of the flight response leads to reduced ability to cope with environmental challenges, a drastic lifespan reduction, and an increase in disease susceptibility. We showed that, in C. elegans, the tyraminergic neuron RIM supplies a state- dependent neural switch between acute flight and long-term environmental stress responses. During the flight-stress response RIM neurons release TA, which stimulates the intestinal adrenergic-like receptor TYRA-3. This leads to DAF-2/Insulin/IGF- 1 pathway activation and inhibition of cytoprotective mechanisms in the intestine and other tissues. We hypothesized that TYRA-3 stimulates the release of Insulin-Like Peptides (ILPs) from the intestine that can systemically activate the DAF-2 insulin/ IGF1 receptors. We focused on strong agonist ILPs that are expressed in the intestine (INS-3, -4, -6, -32, and DAF-28). We found that ins-3 mutants are resistant to both heat and oxidative stress, much like tyra-3 mutants. Moreover, ins-3 mutants are resistant to the impairment of stress resistance upon exposure to exogenous tyramine. In addition, ins-3;tyra-3 double mutants are as resistant to environmental stress as single mutants, suggesting that both genes act in the same pathway. Since ins-3 is expressed in neurons and the intestine, we performed tissue-specific rescue experiments. We found that expression of ins-3 in the intestine restores stress resistance to wild-type levels. Taken together, our results suggest that intestinal activation of TYRA-3 by the escape neurohormone TA leads to INS-3 release which acts as an endocrine, autocrine, and/or paracrine signal to activate DAF-2 in different tissues. |
publishDate |
2023 |
dc.date.none.fl_str_mv |
2023 |
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/11336/250662 Neural modulation of systemic stress response requires the insulin like-peptide INS-3; Third Latin American Worm Meeting; Valparaiso; Chile; 2023; 42-42 CONICET Digital CONICET |
url |
http://hdl.handle.net/11336/250662 |
identifier_str_mv |
Neural modulation of systemic stress response requires the insulin like-peptide INS-3; Third Latin American Worm Meeting; Valparaiso; Chile; 2023; 42-42 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://cinv.uv.cl/en/3rd-la-worm-meeting/ |
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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 application/pdf application/pdf |
dc.coverage.none.fl_str_mv |
Internacional |
dc.publisher.none.fl_str_mv |
Latin American worm meeting |
publisher.none.fl_str_mv |
Latin American worm meeting |
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reponame:CONICET Digital (CONICET) instname:Consejo Nacional de Investigaciones Científicas y Técnicas |
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CONICET Digital (CONICET) |
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Consejo Nacional de Investigaciones Científicas y Técnicas |
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CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas |
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dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar |
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13.070432 |