An insulin like-peptide, INS-3, bridges neural perception of stressors with intracellular defensive mechanisms in non-neuronal cells of C. elegans

Autores
Veuthey, Tania Vanesa; Giunti, Sebastián; Masson, Camila; de Rosa, Maria Jose; Rayes, Diego Hernán
Año de publicación
2018
Idioma
inglés
Tipo de recurso
documento de conferencia
Estado
versión publicada
Descripción
Multicellular organisms coordinate the systemic response to stress. We have shown that in C. elegans the acute-stress response activates neurons that release tyramine (TA), the invertebrate analog of adrenaline/noradrenaline. TA stimulates the DAF-2/Insulin/IGF-1 pathway and precludes the nuclear translocation of the DAF-16/FOXO transcription factor through the activation of an adrenergic-like receptor TYRA-3 in the intestine. In contrast, environmental long-term stressors reduce TA release allowing the induction of FOXO-dependent cytoprotective genes. However, how the insuline and tyraminergic pathway are linked is unknown. We here found that genetic silencing of an insulin like-peptide (ILP) (INS-3) increases the resistance to thermal and oxidative stress, reaching levels similar to tdc-1 (incapable of synthetizing TA) and tyra-3 null mutants. Moreover, unlike wild type animals, exogenous TA does not impair oxidative or thermal stress resistance. In addition, double null mutants between TA- deficient and ILPs null mutants (tdc-1 or tyra-3 with ins-3 or 7) showed levels of stress resistance similar to those found in INS-3 single null mutants, suggesting genetic interaction. Intestinal expression of INS-3 rescues the resistance phenotype of INS-3 null mutants to wild-type levels. We proposed that TA released form the nervous system promotes intestinal release of ILPs, which activate DAF-2 in other cells, inhibiting the systemic stress response mediated by DAF-16/FOXO.
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: Masson, Camila. 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
XXXIII Congreso Anual de la Sociedad Argentina de Investigación en Neurociencias
Cordoba
Argentina
Sociedad Argentina de Investigación en Neurociencias
Materia
Insuline
C. ELEGANS
stress
tyramnine
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:11336/161415

id CONICETDig_3e65ec2f7b154bf5ca6f46616bf80335
oai_identifier_str oai:ri.conicet.gov.ar:11336/161415
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling An insulin like-peptide, INS-3, bridges neural perception of stressors with intracellular defensive mechanisms in non-neuronal cells of C. elegansVeuthey, Tania VanesaGiunti, SebastiánMasson, Camilade Rosa, Maria JoseRayes, Diego HernánInsulineC. ELEGANSstresstyramninehttps://purl.org/becyt/ford/1.6https://purl.org/becyt/ford/1Multicellular organisms coordinate the systemic response to stress. We have shown that in C. elegans the acute-stress response activates neurons that release tyramine (TA), the invertebrate analog of adrenaline/noradrenaline. TA stimulates the DAF-2/Insulin/IGF-1 pathway and precludes the nuclear translocation of the DAF-16/FOXO transcription factor through the activation of an adrenergic-like receptor TYRA-3 in the intestine. In contrast, environmental long-term stressors reduce TA release allowing the induction of FOXO-dependent cytoprotective genes. However, how the insuline and tyraminergic pathway are linked is unknown. We here found that genetic silencing of an insulin like-peptide (ILP) (INS-3) increases the resistance to thermal and oxidative stress, reaching levels similar to tdc-1 (incapable of synthetizing TA) and tyra-3 null mutants. Moreover, unlike wild type animals, exogenous TA does not impair oxidative or thermal stress resistance. In addition, double null mutants between TA- deficient and ILPs null mutants (tdc-1 or tyra-3 with ins-3 or 7) showed levels of stress resistance similar to those found in INS-3 single null mutants, suggesting genetic interaction. Intestinal expression of INS-3 rescues the resistance phenotype of INS-3 null mutants to wild-type levels. We proposed that TA released form the nervous system promotes intestinal release of ILPs, which activate DAF-2 in other cells, inhibiting the systemic stress response mediated by DAF-16/FOXO.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: Masson, Camila. 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; ArgentinaXXXIII Congreso Anual de la Sociedad Argentina de Investigación en NeurocienciasCordobaArgentinaSociedad Argentina de Investigación en NeurocienciasSociedad Argentina de Investigación en Neurociencias2018info: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/11336/161415An insulin like-peptide, INS-3, bridges neural perception of stressors with intracellular defensive mechanisms in non-neuronal cells of C. elegans; XXXIII Congreso Anual de la Sociedad Argentina de Investigación en Neurociencias; Cordoba; Argentina; 2018; 343-343CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://saneurociencias.org.ar/congresos-san-2/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 Técnicas2025-09-29T10:39:33Zoai:ri.conicet.gov.ar:11336/161415instacron: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 10:39:33.434CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv An insulin like-peptide, INS-3, bridges neural perception of stressors with intracellular defensive mechanisms in non-neuronal cells of C. elegans
title An insulin like-peptide, INS-3, bridges neural perception of stressors with intracellular defensive mechanisms in non-neuronal cells of C. elegans
spellingShingle An insulin like-peptide, INS-3, bridges neural perception of stressors with intracellular defensive mechanisms in non-neuronal cells of C. elegans
Veuthey, Tania Vanesa
Insuline
C. ELEGANS
stress
tyramnine
title_short An insulin like-peptide, INS-3, bridges neural perception of stressors with intracellular defensive mechanisms in non-neuronal cells of C. elegans
title_full An insulin like-peptide, INS-3, bridges neural perception of stressors with intracellular defensive mechanisms in non-neuronal cells of C. elegans
title_fullStr An insulin like-peptide, INS-3, bridges neural perception of stressors with intracellular defensive mechanisms in non-neuronal cells of C. elegans
title_full_unstemmed An insulin like-peptide, INS-3, bridges neural perception of stressors with intracellular defensive mechanisms in non-neuronal cells of C. elegans
title_sort An insulin like-peptide, INS-3, bridges neural perception of stressors with intracellular defensive mechanisms in non-neuronal cells of C. elegans
dc.creator.none.fl_str_mv Veuthey, Tania Vanesa
Giunti, Sebastián
Masson, Camila
de Rosa, Maria Jose
Rayes, Diego Hernán
author Veuthey, Tania Vanesa
author_facet Veuthey, Tania Vanesa
Giunti, Sebastián
Masson, Camila
de Rosa, Maria Jose
Rayes, Diego Hernán
author_role author
author2 Giunti, Sebastián
Masson, Camila
de Rosa, Maria Jose
Rayes, Diego Hernán
author2_role author
author
author
author
dc.subject.none.fl_str_mv Insuline
C. ELEGANS
stress
tyramnine
topic Insuline
C. ELEGANS
stress
tyramnine
purl_subject.fl_str_mv https://purl.org/becyt/ford/1.6
https://purl.org/becyt/ford/1
dc.description.none.fl_txt_mv Multicellular organisms coordinate the systemic response to stress. We have shown that in C. elegans the acute-stress response activates neurons that release tyramine (TA), the invertebrate analog of adrenaline/noradrenaline. TA stimulates the DAF-2/Insulin/IGF-1 pathway and precludes the nuclear translocation of the DAF-16/FOXO transcription factor through the activation of an adrenergic-like receptor TYRA-3 in the intestine. In contrast, environmental long-term stressors reduce TA release allowing the induction of FOXO-dependent cytoprotective genes. However, how the insuline and tyraminergic pathway are linked is unknown. We here found that genetic silencing of an insulin like-peptide (ILP) (INS-3) increases the resistance to thermal and oxidative stress, reaching levels similar to tdc-1 (incapable of synthetizing TA) and tyra-3 null mutants. Moreover, unlike wild type animals, exogenous TA does not impair oxidative or thermal stress resistance. In addition, double null mutants between TA- deficient and ILPs null mutants (tdc-1 or tyra-3 with ins-3 or 7) showed levels of stress resistance similar to those found in INS-3 single null mutants, suggesting genetic interaction. Intestinal expression of INS-3 rescues the resistance phenotype of INS-3 null mutants to wild-type levels. We proposed that TA released form the nervous system promotes intestinal release of ILPs, which activate DAF-2 in other cells, inhibiting the systemic stress response mediated by DAF-16/FOXO.
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: Masson, Camila. 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
XXXIII Congreso Anual de la Sociedad Argentina de Investigación en Neurociencias
Cordoba
Argentina
Sociedad Argentina de Investigación en Neurociencias
description Multicellular organisms coordinate the systemic response to stress. We have shown that in C. elegans the acute-stress response activates neurons that release tyramine (TA), the invertebrate analog of adrenaline/noradrenaline. TA stimulates the DAF-2/Insulin/IGF-1 pathway and precludes the nuclear translocation of the DAF-16/FOXO transcription factor through the activation of an adrenergic-like receptor TYRA-3 in the intestine. In contrast, environmental long-term stressors reduce TA release allowing the induction of FOXO-dependent cytoprotective genes. However, how the insuline and tyraminergic pathway are linked is unknown. We here found that genetic silencing of an insulin like-peptide (ILP) (INS-3) increases the resistance to thermal and oxidative stress, reaching levels similar to tdc-1 (incapable of synthetizing TA) and tyra-3 null mutants. Moreover, unlike wild type animals, exogenous TA does not impair oxidative or thermal stress resistance. In addition, double null mutants between TA- deficient and ILPs null mutants (tdc-1 or tyra-3 with ins-3 or 7) showed levels of stress resistance similar to those found in INS-3 single null mutants, suggesting genetic interaction. Intestinal expression of INS-3 rescues the resistance phenotype of INS-3 null mutants to wild-type levels. We proposed that TA released form the nervous system promotes intestinal release of ILPs, which activate DAF-2 in other cells, inhibiting the systemic stress response mediated by DAF-16/FOXO.
publishDate 2018
dc.date.none.fl_str_mv 2018
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/11336/161415
An insulin like-peptide, INS-3, bridges neural perception of stressors with intracellular defensive mechanisms in non-neuronal cells of C. elegans; XXXIII Congreso Anual de la Sociedad Argentina de Investigación en Neurociencias; Cordoba; Argentina; 2018; 343-343
CONICET Digital
CONICET
url http://hdl.handle.net/11336/161415
identifier_str_mv An insulin like-peptide, INS-3, bridges neural perception of stressors with intracellular defensive mechanisms in non-neuronal cells of C. elegans; XXXIII Congreso Anual de la Sociedad Argentina de Investigación en Neurociencias; Cordoba; Argentina; 2018; 343-343
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
application/pdf
application/pdf
dc.coverage.none.fl_str_mv Nacional
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
_version_ 1844614421367750656
score 13.070432