Syntaxin-17 delivers PINK1/parkin-dependent mitochondrial vesicles to the endolysosomal system.
Identifieur interne : 000189 ( PubMed/Corpus ); précédent : 000188; suivant : 000190Syntaxin-17 delivers PINK1/parkin-dependent mitochondrial vesicles to the endolysosomal system.
Auteurs : Gian-Luca Mclelland ; Sydney A. Lee ; Heidi M. Mcbride ; Edward A. FonSource :
- The Journal of cell biology [ 1540-8140 ] ; 2016.
Abstract
Mitochondria are considered autonomous organelles, physically separated from endocytic and biosynthetic pathways. However, recent work uncovered a PINK1/parkin-dependent vesicle transport pathway wherein oxidized or damaged mitochondrial content are selectively delivered to the late endosome/lysosome for degradation, providing evidence that mitochondria are indeed integrated within the endomembrane system. Given that mitochondria have not been shown to use canonical soluble NSF attachment protein receptor (SNARE) machinery for fusion, the mechanism by which mitochondrial-derived vesicles (MDVs) are targeted to the endosomal compartment has remained unclear. In this study, we identify syntaxin-17 as a core mitochondrial SNARE required for the delivery of stress-induced PINK1/parkin-dependent MDVs to the late endosome/lysosome. Syntaxin-17 remains associated with mature MDVs and forms a ternary SNARE complex with SNAP29 and VAMP7 to mediate MDV-endolysosome fusion in a manner dependent on the homotypic fusion and vacuole protein sorting (HOPS) tethering complex. Syntaxin-17 can be traced to the last eukaryotic common ancestor, hinting that the removal of damaged mitochondrial content may represent one of the earliest vesicle transport routes in the cell.
DOI: 10.1083/jcb.201603105
PubMed: 27458136
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Syntaxin-17 delivers PINK1/parkin-dependent mitochondrial vesicles to the endolysosomal system.</title><author><name sortKey="Mclelland, Gian Luca" sort="Mclelland, Gian Luca" uniqKey="Mclelland G" first="Gian-Luca" last="Mclelland">Gian-Luca Mclelland</name><affiliation><nlm:affiliation>McGill Parkinson Program, Montreal Neurological Institute, McGill University, Montreal, Quebec H3A 2B4, Canada Neurodegenerative Diseases Group, Montreal Neurological Institute, McGill University, Montreal, Quebec H3A 2B4, Canada.</nlm:affiliation></affiliation></author><author><name sortKey="Lee, Sydney A" sort="Lee, Sydney A" uniqKey="Lee S" first="Sydney A" last="Lee">Sydney A. Lee</name><affiliation><nlm:affiliation>McGill Parkinson Program, Montreal Neurological Institute, McGill University, Montreal, Quebec H3A 2B4, Canada Neurodegenerative Diseases Group, Montreal Neurological Institute, McGill University, Montreal, Quebec H3A 2B4, Canada.</nlm:affiliation></affiliation></author><author><name sortKey="Mcbride, Heidi M" sort="Mcbride, Heidi M" uniqKey="Mcbride H" first="Heidi M" last="Mcbride">Heidi M. Mcbride</name><affiliation><nlm:affiliation>Rare Diseases Group, Montreal Neurological Institute, McGill University, Montreal, Quebec H3A 2B4, Canada.</nlm:affiliation></affiliation></author><author><name sortKey="Fon, Edward A" sort="Fon, Edward A" uniqKey="Fon E" first="Edward A" last="Fon">Edward A. Fon</name><affiliation><nlm:affiliation>McGill Parkinson Program, Montreal Neurological Institute, McGill University, Montreal, Quebec H3A 2B4, Canada Neurodegenerative Diseases Group, Montreal Neurological Institute, McGill University, Montreal, Quebec H3A 2B4, Canada ted.fon@mcgill.ca.</nlm:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2016">2016</date><idno type="RBID">pubmed:27458136</idno><idno type="pmid">27458136</idno><idno type="doi">10.1083/jcb.201603105</idno><idno type="wicri:Area/PubMed/Corpus">000189</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000189</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Syntaxin-17 delivers PINK1/parkin-dependent mitochondrial vesicles to the endolysosomal system.</title><author><name sortKey="Mclelland, Gian Luca" sort="Mclelland, Gian Luca" uniqKey="Mclelland G" first="Gian-Luca" last="Mclelland">Gian-Luca Mclelland</name><affiliation><nlm:affiliation>McGill Parkinson Program, Montreal Neurological Institute, McGill University, Montreal, Quebec H3A 2B4, Canada Neurodegenerative Diseases Group, Montreal Neurological Institute, McGill University, Montreal, Quebec H3A 2B4, Canada.</nlm:affiliation></affiliation></author><author><name sortKey="Lee, Sydney A" sort="Lee, Sydney A" uniqKey="Lee S" first="Sydney A" last="Lee">Sydney A. Lee</name><affiliation><nlm:affiliation>McGill Parkinson Program, Montreal Neurological Institute, McGill University, Montreal, Quebec H3A 2B4, Canada Neurodegenerative Diseases Group, Montreal Neurological Institute, McGill University, Montreal, Quebec H3A 2B4, Canada.</nlm:affiliation></affiliation></author><author><name sortKey="Mcbride, Heidi M" sort="Mcbride, Heidi M" uniqKey="Mcbride H" first="Heidi M" last="Mcbride">Heidi M. Mcbride</name><affiliation><nlm:affiliation>Rare Diseases Group, Montreal Neurological Institute, McGill University, Montreal, Quebec H3A 2B4, Canada.</nlm:affiliation></affiliation></author><author><name sortKey="Fon, Edward A" sort="Fon, Edward A" uniqKey="Fon E" first="Edward A" last="Fon">Edward A. Fon</name><affiliation><nlm:affiliation>McGill Parkinson Program, Montreal Neurological Institute, McGill University, Montreal, Quebec H3A 2B4, Canada Neurodegenerative Diseases Group, Montreal Neurological Institute, McGill University, Montreal, Quebec H3A 2B4, Canada ted.fon@mcgill.ca.</nlm:affiliation></affiliation></author></analytic><series><title level="j">The Journal of cell biology</title><idno type="eISSN">1540-8140</idno><imprint><date when="2016" type="published">2016</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Mitochondria are considered autonomous organelles, physically separated from endocytic and biosynthetic pathways. However, recent work uncovered a PINK1/parkin-dependent vesicle transport pathway wherein oxidized or damaged mitochondrial content are selectively delivered to the late endosome/lysosome for degradation, providing evidence that mitochondria are indeed integrated within the endomembrane system. Given that mitochondria have not been shown to use canonical soluble NSF attachment protein receptor (SNARE) machinery for fusion, the mechanism by which mitochondrial-derived vesicles (MDVs) are targeted to the endosomal compartment has remained unclear. In this study, we identify syntaxin-17 as a core mitochondrial SNARE required for the delivery of stress-induced PINK1/parkin-dependent MDVs to the late endosome/lysosome. Syntaxin-17 remains associated with mature MDVs and forms a ternary SNARE complex with SNAP29 and VAMP7 to mediate MDV-endolysosome fusion in a manner dependent on the homotypic fusion and vacuole protein sorting (HOPS) tethering complex. Syntaxin-17 can be traced to the last eukaryotic common ancestor, hinting that the removal of damaged mitochondrial content may represent one of the earliest vesicle transport routes in the cell.</div></front></TEI><pubmed><MedlineCitation Status="In-Process" Owner="NLM"><PMID Version="1">27458136</PMID><DateCreated><Year>2016</Year><Month>08</Month><Day>02</Day></DateCreated><DateRevised><Year>2017</Year><Month>02</Month><Day>20</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1540-8140</ISSN><JournalIssue CitedMedium="Internet"><Volume>214</Volume><Issue>3</Issue><PubDate><Year>2016</Year><Month>Aug</Month><Day>01</Day></PubDate></JournalIssue><Title>The Journal of cell biology</Title><ISOAbbreviation>J. Cell Biol.</ISOAbbreviation></Journal><ArticleTitle>Syntaxin-17 delivers PINK1/parkin-dependent mitochondrial vesicles to the endolysosomal system.</ArticleTitle><Pagination><MedlinePgn>275-91</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1083/jcb.201603105</ELocationID><Abstract><AbstractText>Mitochondria are considered autonomous organelles, physically separated from endocytic and biosynthetic pathways. However, recent work uncovered a PINK1/parkin-dependent vesicle transport pathway wherein oxidized or damaged mitochondrial content are selectively delivered to the late endosome/lysosome for degradation, providing evidence that mitochondria are indeed integrated within the endomembrane system. Given that mitochondria have not been shown to use canonical soluble NSF attachment protein receptor (SNARE) machinery for fusion, the mechanism by which mitochondrial-derived vesicles (MDVs) are targeted to the endosomal compartment has remained unclear. In this study, we identify syntaxin-17 as a core mitochondrial SNARE required for the delivery of stress-induced PINK1/parkin-dependent MDVs to the late endosome/lysosome. Syntaxin-17 remains associated with mature MDVs and forms a ternary SNARE complex with SNAP29 and VAMP7 to mediate MDV-endolysosome fusion in a manner dependent on the homotypic fusion and vacuole protein sorting (HOPS) tethering complex. Syntaxin-17 can be traced to the last eukaryotic common ancestor, hinting that the removal of damaged mitochondrial content may represent one of the earliest vesicle transport routes in the cell.</AbstractText><CopyrightInformation>© 2016 McLelland et al.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>McLelland</LastName><ForeName>Gian-Luca</ForeName><Initials>GL</Initials><AffiliationInfo><Affiliation>McGill Parkinson Program, Montreal Neurological Institute, McGill University, Montreal, Quebec H3A 2B4, Canada Neurodegenerative Diseases Group, Montreal Neurological Institute, McGill University, Montreal, Quebec H3A 2B4, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lee</LastName><ForeName>Sydney A</ForeName><Initials>SA</Initials><Identifier Source="ORCID">http://orcid.org/0000-0002-8591-2062</Identifier><AffiliationInfo><Affiliation>McGill Parkinson Program, Montreal Neurological Institute, McGill University, Montreal, Quebec H3A 2B4, Canada Neurodegenerative Diseases Group, Montreal Neurological Institute, McGill University, Montreal, Quebec H3A 2B4, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>McBride</LastName><ForeName>Heidi M</ForeName><Initials>HM</Initials><Identifier Source="ORCID">http://orcid.org/0000-0003-4666-2280</Identifier><AffiliationInfo><Affiliation>Rare Diseases Group, Montreal Neurological Institute, McGill University, Montreal, Quebec H3A 2B4, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Fon</LastName><ForeName>Edward A</ForeName><Initials>EA</Initials><Identifier Source="ORCID">http://orcid.org/0000-0002-5520-6239</Identifier><AffiliationInfo><Affiliation>McGill Parkinson Program, Montreal Neurological Institute, McGill University, Montreal, Quebec H3A 2B4, Canada Neurodegenerative Diseases Group, Montreal Neurological Institute, McGill University, Montreal, Quebec H3A 2B4, Canada ted.fon@mcgill.ca.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><DataBankList CompleteYN="Y"><DataBank><DataBankName>PDB</DataBankName><AccessionNumberList><AccessionNumber>4WY4</AccessionNumber></AccessionNumberList></DataBank></DataBankList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2016</Year><Month>07</Month><Day>25</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J Cell Biol</MedlineTA><NlmUniqueID>0375356</NlmUniqueID><ISSNLinking>0021-9525</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>Biochim Biophys Acta. 2015 Oct;1853(10 Pt B):2797-801</RefSource><PMID Version="1">25634658</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Nature. 2013 Mar 21;495 (7441):389-93</RefSource><PMID 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