A feed-forward mechanism involving the NOX complex and RyR-mediated ca2 + release during axonal specification

Autores
Wilson Rodriguez, Carlos; Munoz-Palma, Ernesto; Henriquez, Daniel R.; Palmisano, Ilaria; Nuñez, Marco Tulio; Di Giovanni, Simone; González Billault, Christian
Año de publicación
2016
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Physiological levels of ROS support neurite outgrowth and axonal specification, but the mechanisms by which ROS are able to shape neurons remain unknown. Ca2 +, a broad intracellular second messenger, promotes both Rac1 activation and neurite extension. Ca2 + release from the endoplasmic reticulum, mediated by both the IP3R1 and ryanodine receptor (RyR) channels, requires physiological ROS levels that are mainly sustained by the NADPH oxidase (NOX) complex. In this work, we explore the contribution of the link between NOX and RyR-mediated Ca2 + release toward axonal specification of rat hippocampal neurons. Using genetic approaches, we find thatNOXactivation promotes both axonal development and Rac1 activation through a RyR-mediated mechanism, which in turn activates NOX through Rac1, one of the NOX subunits. Collectively, these data suggest a feedforward mechanism that integrates both NOX activity and RyR-mediated Ca2 + release to support cellular mechanisms involved in axon development.
Fil: Wilson Rodriguez, Carlos. Universidad de Chile; Chile. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Investigación Médica Mercedes y Martín Ferreyra. Universidad Nacional de Córdoba. Instituto de Investigación Médica Mercedes y Martín Ferreyra; Argentina
Fil: Munoz-Palma, Ernesto. Universidad de Chile; Chile
Fil: Henriquez, Daniel R.. Universidad de Chile; Chile
Fil: Palmisano, Ilaria. Imperial College London; Reino Unido
Fil: Nuñez, Marco Tulio. Universidad de Chile; Chile
Fil: Di Giovanni, Simone. Imperial College London; Reino Unido. University of Tuebingen; Alemania
Fil: González Billault, Christian. Universidad de Chile; Chile
Materia
ACTIN CYTOSKELETON
AXON DEVELOPMENT
CALCIUM SIGNALING
NADPH OXIDASE
NEURONAL DIFFERENTIATION
REACTIVE OXYGEN SPECIES
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:11336/72755
Acceder
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oai_identifier_str oai:ri.conicet.gov.ar:11336/72755
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling A feed-forward mechanism involving the NOX complex and RyR-mediated ca2 + release during axonal specificationWilson Rodriguez, CarlosMunoz-Palma, ErnestoHenriquez, Daniel R.Palmisano, IlariaNuñez, Marco TulioDi Giovanni, SimoneGonzález Billault, ChristianACTIN CYTOSKELETONAXON DEVELOPMENTCALCIUM SIGNALINGNADPH OXIDASENEURONAL DIFFERENTIATIONREACTIVE OXYGEN SPECIEShttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3Physiological levels of ROS support neurite outgrowth and axonal specification, but the mechanisms by which ROS are able to shape neurons remain unknown. Ca2 +, a broad intracellular second messenger, promotes both Rac1 activation and neurite extension. Ca2 + release from the endoplasmic reticulum, mediated by both the IP3R1 and ryanodine receptor (RyR) channels, requires physiological ROS levels that are mainly sustained by the NADPH oxidase (NOX) complex. In this work, we explore the contribution of the link between NOX and RyR-mediated Ca2 + release toward axonal specification of rat hippocampal neurons. Using genetic approaches, we find thatNOXactivation promotes both axonal development and Rac1 activation through a RyR-mediated mechanism, which in turn activates NOX through Rac1, one of the NOX subunits. Collectively, these data suggest a feedforward mechanism that integrates both NOX activity and RyR-mediated Ca2 + release to support cellular mechanisms involved in axon development.Fil: Wilson Rodriguez, Carlos. Universidad de Chile; Chile. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Investigación Médica Mercedes y Martín Ferreyra. Universidad Nacional de Córdoba. Instituto de Investigación Médica Mercedes y Martín Ferreyra; ArgentinaFil: Munoz-Palma, Ernesto. Universidad de Chile; ChileFil: Henriquez, Daniel R.. Universidad de Chile; ChileFil: Palmisano, Ilaria. Imperial College London; Reino UnidoFil: Nuñez, Marco Tulio. Universidad de Chile; ChileFil: Di Giovanni, Simone. Imperial College London; Reino Unido. University of Tuebingen; AlemaniaFil: González Billault, Christian. Universidad de Chile; ChileSociety for Neuroscience2016-10info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/72755Wilson Rodriguez, Carlos; Munoz-Palma, Ernesto; Henriquez, Daniel R.; Palmisano, Ilaria; Nuñez, Marco Tulio; et al.; A feed-forward mechanism involving the NOX complex and RyR-mediated ca2 + release during axonal specification; Society for Neuroscience; Journal of Neuroscience; 36; 43; 10-2016; 11107-111190270-64741529-2401CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/http://www.jneurosci.org/content/36/43/11107info:eu-repo/semantics/altIdentifier/doi/10.1523/JNEUROSCI.1455-16.2016info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-10-15T14:41:13Zoai:ri.conicet.gov.ar:11336/72755instacron: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 14:41:13.465CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv A feed-forward mechanism involving the NOX complex and RyR-mediated ca2 + release during axonal specification
title A feed-forward mechanism involving the NOX complex and RyR-mediated ca2 + release during axonal specification
spellingShingle A feed-forward mechanism involving the NOX complex and RyR-mediated ca2 + release during axonal specification
Wilson Rodriguez, Carlos
ACTIN CYTOSKELETON
AXON DEVELOPMENT
CALCIUM SIGNALING
NADPH OXIDASE
NEURONAL DIFFERENTIATION
REACTIVE OXYGEN SPECIES
title_short A feed-forward mechanism involving the NOX complex and RyR-mediated ca2 + release during axonal specification
title_full A feed-forward mechanism involving the NOX complex and RyR-mediated ca2 + release during axonal specification
title_fullStr A feed-forward mechanism involving the NOX complex and RyR-mediated ca2 + release during axonal specification
title_full_unstemmed A feed-forward mechanism involving the NOX complex and RyR-mediated ca2 + release during axonal specification
title_sort A feed-forward mechanism involving the NOX complex and RyR-mediated ca2 + release during axonal specification
dc.creator.none.fl_str_mv Wilson Rodriguez, Carlos
Munoz-Palma, Ernesto
Henriquez, Daniel R.
Palmisano, Ilaria
Nuñez, Marco Tulio
Di Giovanni, Simone
González Billault, Christian
author Wilson Rodriguez, Carlos
author_facet Wilson Rodriguez, Carlos
Munoz-Palma, Ernesto
Henriquez, Daniel R.
Palmisano, Ilaria
Nuñez, Marco Tulio
Di Giovanni, Simone
González Billault, Christian
author_role author
author2 Munoz-Palma, Ernesto
Henriquez, Daniel R.
Palmisano, Ilaria
Nuñez, Marco Tulio
Di Giovanni, Simone
González Billault, Christian
author2_role author
author
author
author
author
author
dc.subject.none.fl_str_mv ACTIN CYTOSKELETON
AXON DEVELOPMENT
CALCIUM SIGNALING
NADPH OXIDASE
NEURONAL DIFFERENTIATION
REACTIVE OXYGEN SPECIES
topic ACTIN CYTOSKELETON
AXON DEVELOPMENT
CALCIUM SIGNALING
NADPH OXIDASE
NEURONAL DIFFERENTIATION
REACTIVE OXYGEN SPECIES
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.1
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv Physiological levels of ROS support neurite outgrowth and axonal specification, but the mechanisms by which ROS are able to shape neurons remain unknown. Ca2 +, a broad intracellular second messenger, promotes both Rac1 activation and neurite extension. Ca2 + release from the endoplasmic reticulum, mediated by both the IP3R1 and ryanodine receptor (RyR) channels, requires physiological ROS levels that are mainly sustained by the NADPH oxidase (NOX) complex. In this work, we explore the contribution of the link between NOX and RyR-mediated Ca2 + release toward axonal specification of rat hippocampal neurons. Using genetic approaches, we find thatNOXactivation promotes both axonal development and Rac1 activation through a RyR-mediated mechanism, which in turn activates NOX through Rac1, one of the NOX subunits. Collectively, these data suggest a feedforward mechanism that integrates both NOX activity and RyR-mediated Ca2 + release to support cellular mechanisms involved in axon development.
Fil: Wilson Rodriguez, Carlos. Universidad de Chile; Chile. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Investigación Médica Mercedes y Martín Ferreyra. Universidad Nacional de Córdoba. Instituto de Investigación Médica Mercedes y Martín Ferreyra; Argentina
Fil: Munoz-Palma, Ernesto. Universidad de Chile; Chile
Fil: Henriquez, Daniel R.. Universidad de Chile; Chile
Fil: Palmisano, Ilaria. Imperial College London; Reino Unido
Fil: Nuñez, Marco Tulio. Universidad de Chile; Chile
Fil: Di Giovanni, Simone. Imperial College London; Reino Unido. University of Tuebingen; Alemania
Fil: González Billault, Christian. Universidad de Chile; Chile
description Physiological levels of ROS support neurite outgrowth and axonal specification, but the mechanisms by which ROS are able to shape neurons remain unknown. Ca2 +, a broad intracellular second messenger, promotes both Rac1 activation and neurite extension. Ca2 + release from the endoplasmic reticulum, mediated by both the IP3R1 and ryanodine receptor (RyR) channels, requires physiological ROS levels that are mainly sustained by the NADPH oxidase (NOX) complex. In this work, we explore the contribution of the link between NOX and RyR-mediated Ca2 + release toward axonal specification of rat hippocampal neurons. Using genetic approaches, we find thatNOXactivation promotes both axonal development and Rac1 activation through a RyR-mediated mechanism, which in turn activates NOX through Rac1, one of the NOX subunits. Collectively, these data suggest a feedforward mechanism that integrates both NOX activity and RyR-mediated Ca2 + release to support cellular mechanisms involved in axon development.
publishDate 2016
dc.date.none.fl_str_mv 2016-10
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
http://purl.org/coar/resource_type/c_6501
info:ar-repo/semantics/articulo
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv http://hdl.handle.net/11336/72755
Wilson Rodriguez, Carlos; Munoz-Palma, Ernesto; Henriquez, Daniel R.; Palmisano, Ilaria; Nuñez, Marco Tulio; et al.; A feed-forward mechanism involving the NOX complex and RyR-mediated ca2 + release during axonal specification; Society for Neuroscience; Journal of Neuroscience; 36; 43; 10-2016; 11107-11119
0270-6474
1529-2401
CONICET Digital
CONICET
url http://hdl.handle.net/11336/72755
identifier_str_mv Wilson Rodriguez, Carlos; Munoz-Palma, Ernesto; Henriquez, Daniel R.; Palmisano, Ilaria; Nuñez, Marco Tulio; et al.; A feed-forward mechanism involving the NOX complex and RyR-mediated ca2 + release during axonal specification; Society for Neuroscience; Journal of Neuroscience; 36; 43; 10-2016; 11107-11119
0270-6474
1529-2401
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/url/http://www.jneurosci.org/content/36/43/11107
info:eu-repo/semantics/altIdentifier/doi/10.1523/JNEUROSCI.1455-16.2016
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
dc.publisher.none.fl_str_mv Society for Neuroscience
publisher.none.fl_str_mv Society for Neuroscience
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_ 1846082907856175104
score 13.22299

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