The flight response induces the release of an insulin-like peptide from the intestine to inhibit cytoprotective mechanism in C. elegans

Autores
Veuthey, Tania Vanesa; Giunti, Sebastián; de Rosa, Maria Jose; Alkema, Mark J.; Rayes, Diego Hernán
Año de publicación
2020
Idioma
inglés
Tipo de recurso
documento de conferencia
Estado
versión publicada
Descripción
The perpetuation of the flight response inhibits defensive cytoprotective mechanisms, leading to reduced resistance to environmental stressors and shorter lifespan. We recently shown that, in C. elegans, the flight response induces neuronal release of Tyramine (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 intestine and other tissues. However, the signals that bridge intestinal TYRA-3 stimulation with DAF-2 insulin receptor activation in other tissues remain unknown. C. elegans genome encodes 40 Insulin-like peptides (ILPs) that bind to DAF2, 28 of them expressed in the intestine. We test the resistance to environmental stressors (oxidative and thermal stress) silencing individual intestinal ILPs by RNAi. We found that silencing ins-3 improves stress resistance. In contrast to control, exogenous TA addition does not impair stress resistance in ins-3-silenced animals. Moreover, double-null mutants of ins-3 and TA are as resistant to environmental stress as single mutants. This suggests that tyramine and INS-3 act in the same pathway. Since ins-3 is also expressed in neurons, we performed tissue-specific rescues of ins-3 in neuron and intestine to assess the tissue where ins-3 is relevant for controlling stress resistance. Only intestinal ins-3 restores the resistance to wild-type levels. Moreover, stress resistance of ins-3 null-mutants is mediated, at least partially, by DAF-16/FOXO. We propose that intestinal activation of TYRA-3 by the escape neurohormone TA leads to INS-3 release which acts as endocrine, autocrine and/or paracrine signal to activate DAF-2 in the intestine and distal tissues. Given the high degree of conservation of fundamental mechanisms among species, this study can contribute to understanding molecular pathways and cellular communication involved in neural regulation of stress response in multicellular organisms
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: Alkema, Mark J.. University Of Massachussets. Medical School. Department Of Neurobiology; 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. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia; Argentina
2 nd Latin American Worm Meeting
Argentina
Second Latin American Worm meeting
Materia
tyramine
Stress
ILPs
Resistance
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:11336/229463
Acceder
id CONICETDig_0325a1f47565010656604ad3d98a3681
oai_identifier_str oai:ri.conicet.gov.ar:11336/229463
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling The flight response induces the release of an insulin-like peptide from the intestine to inhibit cytoprotective mechanism in C. elegansVeuthey, Tania VanesaGiunti, Sebastiánde Rosa, Maria JoseAlkema, Mark J.Rayes, Diego HernántyramineStressILPsResistancehttps://purl.org/becyt/ford/1.7https://purl.org/becyt/ford/1The perpetuation of the flight response inhibits defensive cytoprotective mechanisms, leading to reduced resistance to environmental stressors and shorter lifespan. We recently shown that, in C. elegans, the flight response induces neuronal release of Tyramine (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 intestine and other tissues. However, the signals that bridge intestinal TYRA-3 stimulation with DAF-2 insulin receptor activation in other tissues remain unknown. C. elegans genome encodes 40 Insulin-like peptides (ILPs) that bind to DAF2, 28 of them expressed in the intestine. We test the resistance to environmental stressors (oxidative and thermal stress) silencing individual intestinal ILPs by RNAi. We found that silencing ins-3 improves stress resistance. In contrast to control, exogenous TA addition does not impair stress resistance in ins-3-silenced animals. Moreover, double-null mutants of ins-3 and TA are as resistant to environmental stress as single mutants. This suggests that tyramine and INS-3 act in the same pathway. Since ins-3 is also expressed in neurons, we performed tissue-specific rescues of ins-3 in neuron and intestine to assess the tissue where ins-3 is relevant for controlling stress resistance. Only intestinal ins-3 restores the resistance to wild-type levels. Moreover, stress resistance of ins-3 null-mutants is mediated, at least partially, by DAF-16/FOXO. We propose that intestinal activation of TYRA-3 by the escape neurohormone TA leads to INS-3 release which acts as endocrine, autocrine and/or paracrine signal to activate DAF-2 in the intestine and distal tissues. Given the high degree of conservation of fundamental mechanisms among species, this study can contribute to understanding molecular pathways and cellular communication involved in neural regulation of stress response in multicellular organismsFil: 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: Alkema, Mark J.. University Of Massachussets. Medical School. Department Of Neurobiology; 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; Argentina. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia; Argentina2 nd Latin American Worm MeetingArgentinaSecond Latin American Worm meetingLatin America.Worm Meeting2020info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/conferenceObjectCongresoBookhttp://purl.org/coar/resource_type/c_5794info:ar-repo/semantics/documentoDeConferenciaapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/229463The flight response induces the release of an insulin-like peptide from the intestine to inhibit cytoprotective mechanism in C. elegans; 2 nd Latin American Worm Meeting; Argentina; 2020; 30-31CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://lawm2020.webnode.es/abstract-submission/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 Técnicas2025-10-22T11:10:26Zoai:ri.conicet.gov.ar:11336/229463instacron: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:34982025-10-22 11:10:26.422CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv The flight response induces the release of an insulin-like peptide from the intestine to inhibit cytoprotective mechanism in C. elegans
title The flight response induces the release of an insulin-like peptide from the intestine to inhibit cytoprotective mechanism in C. elegans
spellingShingle The flight response induces the release of an insulin-like peptide from the intestine to inhibit cytoprotective mechanism in C. elegans
Veuthey, Tania Vanesa
tyramine
Stress
ILPs
Resistance
title_short The flight response induces the release of an insulin-like peptide from the intestine to inhibit cytoprotective mechanism in C. elegans
title_full The flight response induces the release of an insulin-like peptide from the intestine to inhibit cytoprotective mechanism in C. elegans
title_fullStr The flight response induces the release of an insulin-like peptide from the intestine to inhibit cytoprotective mechanism in C. elegans
title_full_unstemmed The flight response induces the release of an insulin-like peptide from the intestine to inhibit cytoprotective mechanism in C. elegans
title_sort The flight response induces the release of an insulin-like peptide from the intestine to inhibit cytoprotective mechanism in C. elegans
dc.creator.none.fl_str_mv Veuthey, Tania Vanesa
Giunti, Sebastián
de Rosa, Maria Jose
Alkema, Mark J.
Rayes, Diego Hernán
author Veuthey, Tania Vanesa
author_facet Veuthey, Tania Vanesa
Giunti, Sebastián
de Rosa, Maria Jose
Alkema, Mark J.
Rayes, Diego Hernán
author_role author
author2 Giunti, Sebastián
de Rosa, Maria Jose
Alkema, Mark J.
Rayes, Diego Hernán
author2_role author
author
author
author
dc.subject.none.fl_str_mv tyramine
Stress
ILPs
Resistance
topic tyramine
Stress
ILPs
Resistance
purl_subject.fl_str_mv https://purl.org/becyt/ford/1.7
https://purl.org/becyt/ford/1
dc.description.none.fl_txt_mv The perpetuation of the flight response inhibits defensive cytoprotective mechanisms, leading to reduced resistance to environmental stressors and shorter lifespan. We recently shown that, in C. elegans, the flight response induces neuronal release of Tyramine (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 intestine and other tissues. However, the signals that bridge intestinal TYRA-3 stimulation with DAF-2 insulin receptor activation in other tissues remain unknown. C. elegans genome encodes 40 Insulin-like peptides (ILPs) that bind to DAF2, 28 of them expressed in the intestine. We test the resistance to environmental stressors (oxidative and thermal stress) silencing individual intestinal ILPs by RNAi. We found that silencing ins-3 improves stress resistance. In contrast to control, exogenous TA addition does not impair stress resistance in ins-3-silenced animals. Moreover, double-null mutants of ins-3 and TA are as resistant to environmental stress as single mutants. This suggests that tyramine and INS-3 act in the same pathway. Since ins-3 is also expressed in neurons, we performed tissue-specific rescues of ins-3 in neuron and intestine to assess the tissue where ins-3 is relevant for controlling stress resistance. Only intestinal ins-3 restores the resistance to wild-type levels. Moreover, stress resistance of ins-3 null-mutants is mediated, at least partially, by DAF-16/FOXO. We propose that intestinal activation of TYRA-3 by the escape neurohormone TA leads to INS-3 release which acts as endocrine, autocrine and/or paracrine signal to activate DAF-2 in the intestine and distal tissues. Given the high degree of conservation of fundamental mechanisms among species, this study can contribute to understanding molecular pathways and cellular communication involved in neural regulation of stress response in multicellular organisms
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: Alkema, Mark J.. University Of Massachussets. Medical School. Department Of Neurobiology; 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. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia; Argentina
2 nd Latin American Worm Meeting
Argentina
Second Latin American Worm meeting
description The perpetuation of the flight response inhibits defensive cytoprotective mechanisms, leading to reduced resistance to environmental stressors and shorter lifespan. We recently shown that, in C. elegans, the flight response induces neuronal release of Tyramine (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 intestine and other tissues. However, the signals that bridge intestinal TYRA-3 stimulation with DAF-2 insulin receptor activation in other tissues remain unknown. C. elegans genome encodes 40 Insulin-like peptides (ILPs) that bind to DAF2, 28 of them expressed in the intestine. We test the resistance to environmental stressors (oxidative and thermal stress) silencing individual intestinal ILPs by RNAi. We found that silencing ins-3 improves stress resistance. In contrast to control, exogenous TA addition does not impair stress resistance in ins-3-silenced animals. Moreover, double-null mutants of ins-3 and TA are as resistant to environmental stress as single mutants. This suggests that tyramine and INS-3 act in the same pathway. Since ins-3 is also expressed in neurons, we performed tissue-specific rescues of ins-3 in neuron and intestine to assess the tissue where ins-3 is relevant for controlling stress resistance. Only intestinal ins-3 restores the resistance to wild-type levels. Moreover, stress resistance of ins-3 null-mutants is mediated, at least partially, by DAF-16/FOXO. We propose that intestinal activation of TYRA-3 by the escape neurohormone TA leads to INS-3 release which acts as endocrine, autocrine and/or paracrine signal to activate DAF-2 in the intestine and distal tissues. Given the high degree of conservation of fundamental mechanisms among species, this study can contribute to understanding molecular pathways and cellular communication involved in neural regulation of stress response in multicellular organisms
publishDate 2020
dc.date.none.fl_str_mv 2020
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/11336/229463
The flight response induces the release of an insulin-like peptide from the intestine to inhibit cytoprotective mechanism in C. elegans; 2 nd Latin American Worm Meeting; Argentina; 2020; 30-31
CONICET Digital
CONICET
url http://hdl.handle.net/11336/229463
identifier_str_mv The flight response induces the release of an insulin-like peptide from the intestine to inhibit cytoprotective mechanism in C. elegans; 2 nd Latin American Worm Meeting; Argentina; 2020; 30-31
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://lawm2020.webnode.es/abstract-submission/
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 Latin America.Worm Meeting
publisher.none.fl_str_mv Latin America.Worm Meeting
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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score 12.982451

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