ParkinsonCanadaV1, Main, Exploration, bibRecord, 001500

ROS-dependent regulation of Parkin and DJ-1 localization during oxidative stress in neurons

Identifieur interne : 001500 ( Main/Exploration ); précédent : 001499; suivant : 001501

ROS-dependent regulation of Parkin and DJ-1 localization during oxidative stress in neurons

Auteurs : Alvin P. Joselin [Canada] ; Sarah J. Hewitt [Canada] ; Steve M. Callaghan [Canada] ; Raymond H. Kim [Canada] ; Young-Hwa Chung [Corée du Sud] ; Tak W. Mak [Canada] ; JIE SHEN [États-Unis] ; Ruth S. Slack [Canada] ; David S. Park [Canada, Corée du Sud]

Source :

Human molecular genetics : (Print) [ 0964-6906 ] ; 2012.

RBID : Pascal:12-0446765

Descripteurs français

Pascal (Inist)
- Régulation, Gène suppresseur tumeur, Protooncogène, Gène onc cellulaire, Localisation, Stress oxydatif, Neurone, Génétique, Gène Parkin, Gène DJ1.
Wicri :
- topic : Génétique.

English descriptors

KwdEn :
- C-Onc gene, Genetics, Localization, Neuron, Oxidative stress, Protooncogene, Regulation(control), Tumor suppressor gene.

Abstract

Mutations in several genes, including Parkin, PTEN-induced kinase 1 (Pink1) and DJ-1, are associated with rare inherited forms of Parkinson's disease (PD). Despite recent attention on the function of these genes, the interplay between DJ-1, Pink1 and Parkin in PD pathogenesis remains unclear. In particular, whether these genes regulate mitochondrial control pathways in neurons is highly controversial. Here we report that Pink1-dependent Parkin translocation does occur in mouse cortical neurons in response to a variety of mitochondrial damaging agents. This translocation only occurs in the absence of antioxidants in the neuronal culturing medium, implicating a key role of reactive oxygen species (ROS) in this response. Consistent with these observations, ROS blockers also prevent Parkin recruitment in mouse embryonic fibroblasts. Loss of DJ-1, a gene linked to ROS management, results in increased stress-induced Parkin recruitment and increased mitophagy. Expression of wild-type DJ-1, but not a cysteine-106 mutant associated with defective ROS response, rescues this accelerated Parkin recruitment. Interestingly, DJ-1 levels increase at mitochondria following oxidative damage in both fibroblasts and neurons, and this process also depends on Parkin and possibly Pink1. These results not only highlight the presence of a Parkin/Pink1-mediated pathway of mitochondrial quality control (MQC) in neurons, they also delineate a complex reciprocal relationship between DJ-1 and the Pink1/Parkin pathway of MQC.

Affiliations:

Canada, Corée du Sud, États-Unis

Links toward previous steps (curation, corpus...)

to stream PascalFrancis, to step Corpus: 000154
to stream PascalFrancis, to step Curation: 000A98
to stream PascalFrancis, to step Checkpoint: 000127
to stream Main, to step Merge: 001541
to stream Main, to step Curation: 001500

Le document en format XML

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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>C-Onc gene</term>
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<term>Oxidative stress</term>
<term>Protooncogene</term>
<term>Regulation(control)</term>
<term>Tumor suppressor gene</term>
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<keywords scheme="Pascal" xml:lang="fr"><term>Régulation</term>
<term>Gène suppresseur tumeur</term>
<term>Protooncogène</term>
<term>Gène onc cellulaire</term>
<term>Localisation</term>
<term>Stress oxydatif</term>
<term>Neurone</term>
<term>Génétique</term>
<term>Gène Parkin</term>
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<front><div type="abstract" xml:lang="en">Mutations in several genes, including Parkin, PTEN-induced kinase 1 (Pink1) and DJ-1, are associated with rare inherited forms of Parkinson's disease (PD). Despite recent attention on the function of these genes, the interplay between DJ-1, Pink1 and Parkin in PD pathogenesis remains unclear. In particular, whether these genes regulate mitochondrial control pathways in neurons is highly controversial. Here we report that Pink1-dependent Parkin translocation does occur in mouse cortical neurons in response to a variety of mitochondrial damaging agents. This translocation only occurs in the absence of antioxidants in the neuronal culturing medium, implicating a key role of reactive oxygen species (ROS) in this response. Consistent with these observations, ROS blockers also prevent Parkin recruitment in mouse embryonic fibroblasts. Loss of DJ-1, a gene linked to ROS management, results in increased stress-induced Parkin recruitment and increased mitophagy. Expression of wild-type DJ-1, but not a cysteine-106 mutant associated with defective ROS response, rescues this accelerated Parkin recruitment. Interestingly, DJ-1 levels increase at mitochondria following oxidative damage in both fibroblasts and neurons, and this process also depends on Parkin and possibly Pink1. These results not only highlight the presence of a Parkin/Pink1-mediated pathway of mitochondrial quality control (MQC) in neurons, they also delineate a complex reciprocal relationship between DJ-1 and the Pink1/Parkin pathway of MQC.</div>
</front>
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	La maladie de Parkinson au Canada (serveur d'exploration)
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La maladie de Parkinson au Canada (serveur d'exploration)

ROS-dependent regulation of Parkin and DJ-1 localization during oxidative stress in neurons

ROS-dependent regulation of Parkin and DJ-1 localization during oxidative stress in neurons

Source :

Descripteurs français

English descriptors

Abstract

Links toward previous steps (curation, corpus...)

Le document en format XML

Pour manipuler ce document sous Unix (Dilib)

Pour mettre un lien sur cette page dans le réseau Wicri