ParkinsonCanadaV1, Pmc, Checkpoint, bibRecord, 000432

Parkin and PINK1 function in a vesicular trafficking pathway regulating mitochondrial quality control

Identifieur interne : 000432 ( Pmc/Checkpoint ); précédent : 000431; suivant : 000433

Parkin and PINK1 function in a vesicular trafficking pathway regulating mitochondrial quality control

Auteurs : Gian-Luca Mclelland [Canada] ; Vincent Soubannier [Canada] ; Carol X. Chen [Canada] ; Heidi M. Mcbride [Canada] ; Edward A. Fon [Canada]

Source :

The EMBO Journal [ 0261-4189 ] ; 2014.

RBID : PMC:3989637

Abstract

Mitochondrial dysfunction has long been associated with Parkinson's disease (PD). Parkin and PINK1, two genes associated with familial PD, have been implicated in the degradation of depolarized mitochondria via autophagy (mitophagy). Here, we describe the involvement of parkin and PINK1 in a vesicular pathway regulating mitochondrial quality control. This pathway is distinct from canonical mitophagy and is triggered by the generation of oxidative stress from within mitochondria. Wild-type but not PD-linked mutant parkin supports the biogenesis of a population of mitochondria-derived vesicles (MDVs), which bud off mitochondria and contain a specific repertoire of cargo proteins. These MDVs require PINK1 expression and ultimately target to lysosomes for degradation. We hypothesize that loss of this parkin- and PINK1-dependent trafficking mechanism impairs the ability of mitochondria to selectively degrade oxidized and damaged proteins leading, over time, to the mitochondrial dysfunction noted in PD.

Url:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3989637

DOI: 10.1002/embj.201385902
PubMed: 24446486
PubMed Central: 3989637

Affiliations:

Canada

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PMC:3989637

Le document en format XML

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<author><name sortKey="Mclelland, Gian Luca" sort="Mclelland, Gian Luca" uniqKey="Mclelland G" first="Gian-Luca" last="Mclelland">Gian-Luca Mclelland</name>
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<addr-line>Montreal, QC, Canada</addr-line>
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<front><div type="abstract" xml:lang="en"><p>Mitochondrial dysfunction has long been associated with Parkinson's disease (PD). <italic>Parkin</italic>
 and <italic>PINK1</italic>
, two genes associated with familial PD, have been implicated in the degradation of depolarized mitochondria via autophagy (mitophagy). Here, we describe the involvement of parkin and PINK1 in a vesicular pathway regulating mitochondrial quality control. This pathway is distinct from canonical mitophagy and is triggered by the generation of oxidative stress from within mitochondria. Wild-type but not PD-linked mutant parkin supports the biogenesis of a population of mitochondria-derived vesicles (MDVs), which bud off mitochondria and contain a specific repertoire of cargo proteins. These MDVs require PINK1 expression and ultimately target to lysosomes for degradation. We hypothesize that loss of this parkin- and PINK1-dependent trafficking mechanism impairs the ability of mitochondria to selectively degrade oxidized and damaged proteins leading, over time, to the mitochondrial dysfunction noted in PD.</p>
</div>
</front>
</TEI>
<pmc article-type="research-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
  <front><journal-meta><journal-id journal-id-type="nlm-ta">EMBO J</journal-id>
<journal-id journal-id-type="iso-abbrev">EMBO J</journal-id>
<journal-id journal-id-type="publisher-id">embj</journal-id>
<journal-title-group><journal-title>The EMBO Journal</journal-title>
</journal-title-group>
<issn pub-type="ppub">0261-4189</issn>
<issn pub-type="epub">1460-2075</issn>
<publisher><publisher-name>BlackWell Publishing Ltd</publisher-name>
<publisher-loc>Oxford, UK</publisher-loc>
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</journal-meta>
<article-meta><article-id pub-id-type="pmid">24446486</article-id>
<article-id pub-id-type="pmc">3989637</article-id>
<article-id pub-id-type="doi">10.1002/embj.201385902</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Articles</subject>
</subj-group>
</article-categories>
<title-group><article-title>Parkin and PINK1 function in a vesicular trafficking pathway regulating mitochondrial quality control</article-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>McLelland</surname>
<given-names>Gian-Luca</given-names>
</name>
<xref ref-type="aff" rid="au1">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Soubannier</surname>
<given-names>Vincent</given-names>
</name>
<xref ref-type="aff" rid="au2">2</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Chen</surname>
<given-names>Carol X</given-names>
</name>
<xref ref-type="aff" rid="au1">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>McBride</surname>
<given-names>Heidi M</given-names>
</name>
<xref ref-type="aff" rid="au2">2</xref>
<xref ref-type="corresp" rid="cor2">**</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Fon</surname>
<given-names>Edward A</given-names>
</name>
<xref ref-type="aff" rid="au1">1</xref>
<xref ref-type="corresp" rid="cor1">*</xref>
</contrib>
<aff id="au1"><label>1</label>
<institution>McGill Parkinson Program, Department of Neurology and Neurosurgery, Montreal Neurological Institute and Hospital, McGill University</institution>
<addr-line>Montreal, QC, Canada</addr-line>
</aff>
<aff id="au2"><label>2</label>
<institution>Neuromuscular Group, Department of Neurology and Neurosurgery, Montreal Neurological Institute and Hospital, McGill University</institution>
<addr-line>Montreal, QC, Canada</addr-line>
</aff>
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<author-notes><corresp id="cor1">* Corresponding author. Tel: +514 398 8398; Fax: +514 398 5214; E-mail: <email>ted.fon@mcgill.ca</email>
</corresp>
<corresp id="cor2">** Corresponding author. Tel: +514 398 1808; Fax: +514 398 1509; E-mail: <email>heidi.mcbride@mcgill.ca</email>
</corresp>
<fn><p><bold>Subject Categories</bold>
 Membrane & Intracellular Transport</p>
</fn>
</author-notes>
<pub-date pub-type="ppub"><day>18</day>
<month>2</month>
<year>2014</year>
</pub-date>
<pub-date pub-type="epub"><day>20</day>
<month>1</month>
<year>2014</year>
</pub-date>
<volume>33</volume>
<issue>4</issue>
<fpage>282</fpage>
<lpage>295</lpage>
<history><date date-type="received"><day>05</day>
<month>6</month>
<year>2013</year>
</date>
<date date-type="rev-recd"><day>24</day>
<month>10</month>
<year>2013</year>
</date>
<date date-type="accepted"><day>05</day>
<month>12</month>
<year>2013</year>
</date>
</history>
<permissions><copyright-statement>© 2014 The Authors</copyright-statement>
<copyright-year>2014</copyright-year>
</permissions>
<related-article related-article-type="companion" id="d35e149" vol="33" page="277" xlink:href="24502976" ext-link-type="pubmed"></related-article>
<abstract><p>Mitochondrial dysfunction has long been associated with Parkinson's disease (PD). <italic>Parkin</italic>
 and <italic>PINK1</italic>
, two genes associated with familial PD, have been implicated in the degradation of depolarized mitochondria via autophagy (mitophagy). Here, we describe the involvement of parkin and PINK1 in a vesicular pathway regulating mitochondrial quality control. This pathway is distinct from canonical mitophagy and is triggered by the generation of oxidative stress from within mitochondria. Wild-type but not PD-linked mutant parkin supports the biogenesis of a population of mitochondria-derived vesicles (MDVs), which bud off mitochondria and contain a specific repertoire of cargo proteins. These MDVs require PINK1 expression and ultimately target to lysosomes for degradation. We hypothesize that loss of this parkin- and PINK1-dependent trafficking mechanism impairs the ability of mitochondria to selectively degrade oxidized and damaged proteins leading, over time, to the mitochondrial dysfunction noted in PD.</p>
</abstract>
<kwd-group><kwd>MDV</kwd>
<kwd>mitochondria</kwd>
<kwd>mitophagy</kwd>
<kwd>Parkin</kwd>
<kwd>PINK1</kwd>
</kwd-group>
</article-meta>
</front>
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<affiliations><list><country><li>Canada</li>
</country>
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<tree><country name="Canada"><noRegion><name sortKey="Mclelland, Gian Luca" sort="Mclelland, Gian Luca" uniqKey="Mclelland G" first="Gian-Luca" last="Mclelland">Gian-Luca Mclelland</name>
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<name sortKey="Chen, Carol X" sort="Chen, Carol X" uniqKey="Chen C" first="Carol X" last="Chen">Carol X. Chen</name>
<name sortKey="Fon, Edward A" sort="Fon, Edward A" uniqKey="Fon E" first="Edward A" last="Fon">Edward A. Fon</name>
<name sortKey="Mcbride, Heidi M" sort="Mcbride, Heidi M" uniqKey="Mcbride H" first="Heidi M" last="Mcbride">Heidi M. Mcbride</name>
<name sortKey="Soubannier, Vincent" sort="Soubannier, Vincent" uniqKey="Soubannier V" first="Vincent" last="Soubannier">Vincent Soubannier</name>
</country>
</tree>
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</record>

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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)

Parkin and PINK1 function in a vesicular trafficking pathway regulating mitochondrial quality control

Parkin and PINK1 function in a vesicular trafficking pathway regulating mitochondrial quality control

Source :

Abstract

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

Links to Exploration step

Le document en format XML

Pour manipuler ce document sous Unix (Dilib)

Pour mettre un lien sur cette page dans le réseau Wicri

Pour générer des pages wiki