SLC35D3 increases autophagic activity in midbrain dopaminergic neurons by enhancing BECN1-ATG14-PIK3C3 complex formation.
Identifieur interne : 000118 ( PubMed/Corpus ); précédent : 000117; suivant : 000119SLC35D3 increases autophagic activity in midbrain dopaminergic neurons by enhancing BECN1-ATG14-PIK3C3 complex formation.
Auteurs : Zong-Bo Wei ; Ye-Feng Yuan ; Florence Jaouen ; Mei-Sheng Ma ; Chan-Juan Hao ; Zhe Zhang ; Quan Chen ; Zengqiang Yuan ; Li Yu ; Corinne Beurrier ; Wei LiSource :
- Autophagy [ 1554-8635 ] ; 2016.
Abstract
Searching for new regulators of autophagy involved in selective dopaminergic (DA) neuron loss is a hallmark in the pathogenesis of Parkinson disease (PD). We here report that an endoplasmic reticulum (ER)-associated transmembrane protein SLC35D3 is selectively expressed in subsets of midbrain DA neurons in about 10% TH (tyrosine hydroxylase)-positive neurons in the substantia nigra pars compacta (SNc) and in about 22% TH-positive neurons in the ventral tegmental area (VTA). Loss of SLC35D3 in ros (roswell mutant) mice showed a reduction of 11.9% DA neurons in the SNc and 15.5% DA neuron loss in the VTA with impaired autophagy. We determined that SLC35D3 enhanced the formation of the BECN1-ATG14-PIK3C3 complex to induce autophagy. These results suggest that SLC35D3 is a new regulator of tissue-specific autophagy and plays an important role in the increased autophagic activity required for the survival of subsets of DA neurons.
DOI: 10.1080/15548627.2016.1179402
PubMed: 27171858
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last="Jaouen">Florence Jaouen</name><affiliation><nlm:affiliation>c Aix-Marseille University, Center National de la Recherche Scientifique , UMR 7288 , Institut de Biologie du Développement de Marseille, Marseille , France.</nlm:affiliation></affiliation></author><author><name sortKey="Ma, Mei Sheng" sort="Ma, Mei Sheng" uniqKey="Ma M" first="Mei-Sheng" last="Ma">Mei-Sheng Ma</name><affiliation><nlm:affiliation>d School of Life Sciences, Tsinghua University , Beijing , China.</nlm:affiliation></affiliation></author><author><name sortKey="Hao, Chan Juan" sort="Hao, Chan Juan" uniqKey="Hao C" first="Chan-Juan" last="Hao">Chan-Juan Hao</name><affiliation><nlm:affiliation>a State Key Laboratory of Molecular Developmental Biology, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences , Beijing , China.</nlm:affiliation></affiliation></author><author><name sortKey="Zhang, Zhe" sort="Zhang, Zhe" uniqKey="Zhang Z" first="Zhe" last="Zhang">Zhe Zhang</name><affiliation><nlm:affiliation>a State Key Laboratory of Molecular Developmental Biology, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences , Beijing , China.</nlm:affiliation></affiliation></author><author><name sortKey="Chen, Quan" sort="Chen, Quan" uniqKey="Chen Q" first="Quan" last="Chen">Quan Chen</name><affiliation><nlm:affiliation>f Institute of Zoology, Chinese Academy of Sciences , Beijing , China.</nlm:affiliation></affiliation></author><author><name sortKey="Yuan, Zengqiang" sort="Yuan, Zengqiang" uniqKey="Yuan Z" first="Zengqiang" last="Yuan">Zengqiang Yuan</name><affiliation><nlm:affiliation>g Institute of Biophysics, Chinese Academy of Sciences , Beijing , China.</nlm:affiliation></affiliation></author><author><name sortKey="Yu, Li" sort="Yu, Li" uniqKey="Yu L" first="Li" last="Yu">Li Yu</name><affiliation><nlm:affiliation>d School of Life Sciences, Tsinghua University , Beijing , China.</nlm:affiliation></affiliation></author><author><name sortKey="Beurrier, Corinne" sort="Beurrier, Corinne" uniqKey="Beurrier C" first="Corinne" last="Beurrier">Corinne Beurrier</name><affiliation><nlm:affiliation>c Aix-Marseille University, Center National de la Recherche Scientifique , UMR 7288 , Institut de Biologie du Développement de Marseille, Marseille , France.</nlm:affiliation></affiliation></author><author><name sortKey="Li, Wei" sort="Li, Wei" uniqKey="Li W" first="Wei" last="Li">Wei Li</name><affiliation><nlm:affiliation>a State Key Laboratory of Molecular Developmental Biology, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences , Beijing , China.</nlm:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2016">2016</date><idno type="RBID">pubmed:27171858</idno><idno type="pmid">27171858</idno><idno type="doi">10.1080/15548627.2016.1179402</idno><idno 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China.</nlm:affiliation></affiliation></author><author><name sortKey="Jaouen, Florence" sort="Jaouen, Florence" uniqKey="Jaouen F" first="Florence" last="Jaouen">Florence Jaouen</name><affiliation><nlm:affiliation>c Aix-Marseille University, Center National de la Recherche Scientifique , UMR 7288 , Institut de Biologie du Développement de Marseille, Marseille , France.</nlm:affiliation></affiliation></author><author><name sortKey="Ma, Mei Sheng" sort="Ma, Mei Sheng" uniqKey="Ma M" first="Mei-Sheng" last="Ma">Mei-Sheng Ma</name><affiliation><nlm:affiliation>d School of Life Sciences, Tsinghua University , Beijing , China.</nlm:affiliation></affiliation></author><author><name sortKey="Hao, Chan Juan" sort="Hao, Chan Juan" uniqKey="Hao C" first="Chan-Juan" last="Hao">Chan-Juan Hao</name><affiliation><nlm:affiliation>a State Key Laboratory of Molecular Developmental Biology, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences , Beijing , China.</nlm:affiliation></affiliation></author><author><name sortKey="Zhang, Zhe" sort="Zhang, Zhe" uniqKey="Zhang Z" first="Zhe" last="Zhang">Zhe Zhang</name><affiliation><nlm:affiliation>a State Key Laboratory of Molecular Developmental Biology, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences , Beijing , China.</nlm:affiliation></affiliation></author><author><name sortKey="Chen, Quan" sort="Chen, Quan" uniqKey="Chen Q" first="Quan" last="Chen">Quan Chen</name><affiliation><nlm:affiliation>f Institute of Zoology, Chinese Academy of Sciences , Beijing , China.</nlm:affiliation></affiliation></author><author><name sortKey="Yuan, Zengqiang" sort="Yuan, Zengqiang" uniqKey="Yuan Z" first="Zengqiang" last="Yuan">Zengqiang Yuan</name><affiliation><nlm:affiliation>g Institute of Biophysics, Chinese Academy of Sciences , Beijing , China.</nlm:affiliation></affiliation></author><author><name sortKey="Yu, Li" sort="Yu, Li" uniqKey="Yu L" first="Li" last="Yu">Li Yu</name><affiliation><nlm:affiliation>d School of Life Sciences, Tsinghua University , Beijing , China.</nlm:affiliation></affiliation></author><author><name sortKey="Beurrier, Corinne" sort="Beurrier, Corinne" uniqKey="Beurrier C" first="Corinne" last="Beurrier">Corinne Beurrier</name><affiliation><nlm:affiliation>c Aix-Marseille University, Center National de la Recherche Scientifique , UMR 7288 , Institut de Biologie du Développement de Marseille, Marseille , France.</nlm:affiliation></affiliation></author><author><name sortKey="Li, Wei" sort="Li, Wei" uniqKey="Li W" first="Wei" last="Li">Wei Li</name><affiliation><nlm:affiliation>a State Key Laboratory of Molecular Developmental Biology, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences , Beijing , China.</nlm:affiliation></affiliation></author></analytic><series><title level="j">Autophagy</title><idno type="eISSN">1554-8635</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">Searching for new regulators of autophagy involved in selective dopaminergic (DA) neuron loss is a hallmark in the pathogenesis of Parkinson disease (PD). We here report that an endoplasmic reticulum (ER)-associated transmembrane protein SLC35D3 is selectively expressed in subsets of midbrain DA neurons in about 10% TH (tyrosine hydroxylase)-positive neurons in the substantia nigra pars compacta (SNc) and in about 22% TH-positive neurons in the ventral tegmental area (VTA). Loss of SLC35D3 in ros (roswell mutant) mice showed a reduction of 11.9% DA neurons in the SNc and 15.5% DA neuron loss in the VTA with impaired autophagy. We determined that SLC35D3 enhanced the formation of the BECN1-ATG14-PIK3C3 complex to induce autophagy. These results suggest that SLC35D3 is a new regulator of tissue-specific autophagy and plays an important role in the increased autophagic activity required for the survival of subsets of DA neurons.</div></front></TEI><pubmed><MedlineCitation Status="In-Data-Review" Owner="NLM"><PMID Version="1">27171858</PMID><DateCreated><Year>2016</Year><Month>07</Month><Day>07</Day></DateCreated><DateRevised><Year>2016</Year><Month>08</Month><Day>26</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1554-8635</ISSN><JournalIssue CitedMedium="Internet"><Volume>12</Volume><Issue>7</Issue><PubDate><Year>2016</Year><Month>Jul</Month><Day>02</Day></PubDate></JournalIssue><Title>Autophagy</Title><ISOAbbreviation>Autophagy</ISOAbbreviation></Journal><ArticleTitle>SLC35D3 increases autophagic activity in midbrain dopaminergic neurons by enhancing BECN1-ATG14-PIK3C3 complex formation.</ArticleTitle><Pagination><MedlinePgn>1168-79</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1080/15548627.2016.1179402</ELocationID><Abstract><AbstractText>Searching for new regulators of autophagy involved in selective dopaminergic (DA) neuron loss is a hallmark in the pathogenesis of Parkinson disease (PD). We here report that an endoplasmic reticulum (ER)-associated transmembrane protein SLC35D3 is selectively expressed in subsets of midbrain DA neurons in about 10% TH (tyrosine hydroxylase)-positive neurons in the substantia nigra pars compacta (SNc) and in about 22% TH-positive neurons in the ventral tegmental area (VTA). Loss of SLC35D3 in ros (roswell mutant) mice showed a reduction of 11.9% DA neurons in the SNc and 15.5% DA neuron loss in the VTA with impaired autophagy. We determined that SLC35D3 enhanced the formation of the BECN1-ATG14-PIK3C3 complex to induce autophagy. These results suggest that SLC35D3 is a new regulator of tissue-specific autophagy and plays an important role in the increased autophagic activity required for the survival of subsets of DA neurons.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Wei</LastName><ForeName>Zong-Bo</ForeName><Initials>ZB</Initials><AffiliationInfo><Affiliation>a State Key Laboratory of Molecular Developmental Biology, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences , Beijing , China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>b University of Chinese Academy of Sciences , Beijing , China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yuan</LastName><ForeName>Ye-Feng</ForeName><Initials>YF</Initials><AffiliationInfo><Affiliation>a State Key Laboratory of Molecular Developmental Biology, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences , Beijing , China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>b University of Chinese Academy of Sciences , Beijing , China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Jaouen</LastName><ForeName>Florence</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>c Aix-Marseille University, Center National de la Recherche Scientifique , UMR 7288 , Institut de Biologie du Développement de Marseille, Marseille , France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ma</LastName><ForeName>Mei-Sheng</ForeName><Initials>MS</Initials><AffiliationInfo><Affiliation>d School of Life Sciences, Tsinghua University , Beijing , China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hao</LastName><ForeName>Chan-Juan</ForeName><Initials>CJ</Initials><AffiliationInfo><Affiliation>a State Key Laboratory of Molecular Developmental Biology, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences , Beijing , China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>e Center for Medical Genetics, Beijing Children's Hospital, Capital Medical University, Beijing Pediatric Research Institute , Beijing , China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Zhe</ForeName><Initials>Z</Initials><AffiliationInfo><Affiliation>a State Key Laboratory of Molecular Developmental Biology, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences , Beijing , China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chen</LastName><ForeName>Quan</ForeName><Initials>Q</Initials><AffiliationInfo><Affiliation>f Institute of Zoology, Chinese Academy of Sciences , Beijing , China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yuan</LastName><ForeName>Zengqiang</ForeName><Initials>Z</Initials><AffiliationInfo><Affiliation>g Institute of Biophysics, Chinese Academy of Sciences , Beijing , China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yu</LastName><ForeName>Li</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>d School of Life Sciences, Tsinghua University , Beijing , China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Beurrier</LastName><ForeName>Corinne</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>c Aix-Marseille University, Center National de la Recherche Scientifique , UMR 7288 , Institut de Biologie du Développement de Marseille, Marseille , France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Wei</ForeName><Initials>W</Initials><AffiliationInfo><Affiliation>a State Key Laboratory of Molecular Developmental Biology, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences , Beijing , China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>e Center for Medical Genetics, Beijing Children's Hospital, Capital Medical University, Beijing Pediatric Research Institute , Beijing , China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>h Center of Alzheimer Disease, Beijing Institute for Brain Disorders , Beijing , China.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2016</Year><Month>05</Month><Day>12</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Autophagy</MedlineTA><NlmUniqueID>101265188</NlmUniqueID><ISSNLinking>1554-8627</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><OtherID Source="NLM">PMC4990987 [Available on 05/12/17]</OtherID><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">BECN1-ATG14-PIK3C3 complex</Keyword><Keyword MajorTopicYN="N">Parkinson disease</Keyword><Keyword MajorTopicYN="N">SLC35D3</Keyword><Keyword MajorTopicYN="N">autophagy</Keyword><Keyword MajorTopicYN="N">dopaminergic neuron</Keyword><Keyword MajorTopicYN="N">neurodegeneration</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pmc-release"><Year>2017</Year><Month>05</Month><Day>12</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2016</Year><Month>5</Month><Day>13</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2016</Year><Month>5</Month><Day>14</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2016</Year><Month>5</Month><Day>14</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">27171858</ArticleId><ArticleId IdType="doi">10.1080/15548627.2016.1179402</ArticleId><ArticleId 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