SLC35D3 increases autophagic activity in midbrain dopaminergic neurons by enhancing BECN1-ATG14-PIK3C3 complex formation.
Identifieur interne : 000166 ( Main/Exploration ); précédent : 000165; suivant : 000167SLC35D3 increases autophagic activity in midbrain dopaminergic neurons by enhancing BECN1-ATG14-PIK3C3 complex formation.
Auteurs : Zong-Bo Wei [République populaire de Chine] ; Ye-Feng Yuan [République populaire de Chine] ; Florence Jaouen [France] ; Mei-Sheng Ma [République populaire de Chine] ; Chan-Juan Hao [République populaire de Chine] ; Zhe Zhang [République populaire de Chine] ; Quan Chen [République populaire de Chine] ; Zengqiang Yuan [République populaire de Chine] ; Li Yu [République populaire de Chine] ; Corinne Beurrier [France] ; Wei Li [République populaire de Chine]Source :
- 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
Affiliations:
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uniqKey="Wei Z" first="Zong-Bo" last="Wei">Zong-Bo Wei</name><affiliation wicri:level="1"><nlm:affiliation>a State Key Laboratory of Molecular Developmental Biology, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences , Beijing , China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>a State Key Laboratory of Molecular Developmental Biology, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences , Beijing </wicri:regionArea><wicri:noRegion>Beijing </wicri:noRegion></affiliation></author><author><name sortKey="Yuan, Ye Feng" sort="Yuan, Ye Feng" uniqKey="Yuan Y" first="Ye-Feng" last="Yuan">Ye-Feng Yuan</name><affiliation wicri:level="1"><nlm:affiliation>a State Key Laboratory of Molecular Developmental Biology, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences , Beijing , China.</nlm:affiliation><country xml:lang="fr">République populaire de 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Mei Sheng" uniqKey="Ma M" first="Mei-Sheng" last="Ma">Mei-Sheng Ma</name><affiliation wicri:level="1"><nlm:affiliation>d School of Life Sciences, Tsinghua University , Beijing , China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>d School of Life Sciences, Tsinghua University , Beijing </wicri:regionArea><wicri:noRegion>Beijing </wicri:noRegion></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 wicri:level="1"><nlm:affiliation>a State Key Laboratory of Molecular Developmental Biology, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences , Beijing , China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>a State Key Laboratory of Molecular Developmental Biology, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences , Beijing </wicri:regionArea><wicri:noRegion>Beijing </wicri:noRegion></affiliation></author><author><name sortKey="Zhang, Zhe" sort="Zhang, Zhe" uniqKey="Zhang Z" first="Zhe" last="Zhang">Zhe Zhang</name><affiliation wicri:level="1"><nlm:affiliation>a State Key Laboratory of Molecular Developmental Biology, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences , Beijing , China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>a State Key Laboratory of Molecular Developmental Biology, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences , Beijing </wicri:regionArea><wicri:noRegion>Beijing </wicri:noRegion></affiliation></author><author><name sortKey="Chen, Quan" sort="Chen, Quan" uniqKey="Chen Q" first="Quan" last="Chen">Quan Chen</name><affiliation wicri:level="1"><nlm:affiliation>f Institute of Zoology, Chinese Academy of Sciences , Beijing , China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>f Institute of Zoology, Chinese Academy of Sciences , Beijing </wicri:regionArea><wicri:noRegion>Beijing </wicri:noRegion></affiliation></author><author><name sortKey="Yuan, Zengqiang" sort="Yuan, Zengqiang" uniqKey="Yuan Z" first="Zengqiang" last="Yuan">Zengqiang Yuan</name><affiliation wicri:level="1"><nlm:affiliation>g Institute of Biophysics, Chinese Academy of Sciences , Beijing , China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>g Institute of Biophysics, Chinese Academy of Sciences , Beijing </wicri:regionArea><wicri:noRegion>Beijing </wicri:noRegion></affiliation></author><author><name sortKey="Yu, Li" sort="Yu, Li" uniqKey="Yu L" first="Li" last="Yu">Li Yu</name><affiliation wicri:level="1"><nlm:affiliation>d School of Life Sciences, Tsinghua University , Beijing , China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>d School of Life Sciences, Tsinghua University , Beijing </wicri:regionArea><wicri:noRegion>Beijing </wicri:noRegion></affiliation></author><author><name sortKey="Beurrier, Corinne" sort="Beurrier, Corinne" uniqKey="Beurrier C" first="Corinne" last="Beurrier">Corinne Beurrier</name><affiliation wicri:level="1"><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><country xml:lang="fr">France</country><wicri:regionArea>c Aix-Marseille University, Center National de la Recherche Scientifique , UMR 7288 , Institut de Biologie du Développement de Marseille, Marseille </wicri:regionArea><wicri:noRegion>Marseille </wicri:noRegion><wicri:noRegion>Marseille </wicri:noRegion></affiliation></author><author><name sortKey="Li, Wei" sort="Li, Wei" uniqKey="Li W" first="Wei" last="Li">Wei Li</name><affiliation wicri:level="1"><nlm:affiliation>a State Key Laboratory of Molecular Developmental Biology, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences , Beijing , China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>a State Key Laboratory of Molecular Developmental Biology, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences , Beijing </wicri:regionArea><wicri:noRegion>Beijing </wicri:noRegion></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><affiliations><list><country><li>France</li><li>République populaire de Chine</li></country></list><tree><country name="République populaire de Chine"><noRegion><name sortKey="Wei, Zong Bo" sort="Wei, Zong Bo" uniqKey="Wei Z" first="Zong-Bo" last="Wei">Zong-Bo Wei</name></noRegion><name sortKey="Chen, Quan" sort="Chen, Quan" uniqKey="Chen Q" first="Quan" last="Chen">Quan Chen</name><name sortKey="Hao, Chan Juan" sort="Hao, Chan Juan" uniqKey="Hao C" first="Chan-Juan" last="Hao">Chan-Juan Hao</name><name sortKey="Li, Wei" sort="Li, Wei" uniqKey="Li W" first="Wei" last="Li">Wei Li</name><name sortKey="Ma, Mei Sheng" sort="Ma, Mei Sheng" uniqKey="Ma M" first="Mei-Sheng" last="Ma">Mei-Sheng Ma</name><name sortKey="Yu, Li" sort="Yu, Li" uniqKey="Yu L" first="Li" last="Yu">Li Yu</name><name sortKey="Yuan, Ye Feng" sort="Yuan, Ye Feng" uniqKey="Yuan Y" first="Ye-Feng" last="Yuan">Ye-Feng Yuan</name><name sortKey="Yuan, Zengqiang" sort="Yuan, Zengqiang" uniqKey="Yuan Z" first="Zengqiang" last="Yuan">Zengqiang Yuan</name><name sortKey="Zhang, Zhe" sort="Zhang, Zhe" uniqKey="Zhang Z" first="Zhe" last="Zhang">Zhe Zhang</name></country><country name="France"><noRegion><name sortKey="Jaouen, Florence" sort="Jaouen, Florence" uniqKey="Jaouen F" first="Florence" last="Jaouen">Florence Jaouen</name></noRegion><name sortKey="Beurrier, Corinne" sort="Beurrier, Corinne" uniqKey="Beurrier C" first="Corinne" last="Beurrier">Corinne Beurrier</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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