A Saccharomyces cerevisiae strain unable to store neutral lipids is tolerant to oxidative stress induced by α-synuclein.
Identifieur interne : 000A49 ( PubMed/Checkpoint ); précédent : 000A48; suivant : 000A50A Saccharomyces cerevisiae strain unable to store neutral lipids is tolerant to oxidative stress induced by α-synuclein.
Auteurs : Yves Y. Sere [France] ; Matthieu Regnacq ; Jenny Colas ; Thierry BergesSource :
- Free radical biology & medicine [ 1873-4596 ] ; 2010.
English descriptors
- KwdEn :
- Adaptation, Biological (drug effects), Adaptation, Biological (genetics), Drug Resistance (genetics), Enzyme Activation (drug effects), Fatty Acid Synthases (metabolism), Glutathione (metabolism), Lipid Metabolism (genetics), Lipid Metabolism Disorders (genetics), Lipid Metabolism Disorders (pathology), Models, Theoretical, Organisms, Genetically Modified, Oxidation-Reduction (drug effects), Oxidative Stress (drug effects), Oxidative Stress (genetics), Oxidative Stress (physiology), Saccharomyces cerevisiae (genetics), Saccharomyces cerevisiae (growth & development), Saccharomyces cerevisiae (metabolism), Squalene (metabolism), alpha-Synuclein (genetics), alpha-Synuclein (metabolism), alpha-Synuclein (pharmacology), alpha-Synuclein (physiology).
- MESH :
- chemical , genetics : alpha-Synuclein.
- chemical , metabolism : Fatty Acid Synthases, Glutathione, Squalene, alpha-Synuclein.
- drug effects : Adaptation, Biological, Enzyme Activation, Oxidation-Reduction, Oxidative Stress.
- genetics : Adaptation, Biological, Drug Resistance, Lipid Metabolism, Lipid Metabolism Disorders, Oxidative Stress, Saccharomyces cerevisiae.
- growth & development : Saccharomyces cerevisiae.
- metabolism : Saccharomyces cerevisiae.
- pathology : Lipid Metabolism Disorders.
- chemical , pharmacology : alpha-Synuclein.
- physiology : Oxidative Stress, alpha-Synuclein.
- Models, Theoretical, Organisms, Genetically Modified.
Abstract
Parkinson disease is a neurodegenerative pathology that has been linked to several genetic mutations of the SNCA gene encoding the pro-oxidant α-synuclein protein. The budding yeast Saccharomyces cerevisiae is a valuable model for studying the cellular and molecular mechanisms of α-synuclein toxicity. Indeed heterologous expression of α-synuclein is toxic to wild-type yeast and exhibits the main features of damage caused to mammalian neurons, including an increase in neutral lipid storage (triglycerides and steryl esters, embedded into lipid droplets). To address the significance of this accumulation, we forced α-synuclein production in a strain unable to synthesize triglycerides and steryl esters. Surprisingly, the inability to store neutral lipids rendered the cells more tolerant to α-synuclein. Our results indicate that the level of α-synuclein toxicity is correlated with fatty acid synthase activity and intracellular redox status.
DOI: 10.1016/j.freeradbiomed.2010.09.007
PubMed: 20850523
Affiliations:
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Sere</name><affiliation wicri:level="4"><nlm:affiliation>CNRS-UMR6187, Institut de Physiologie et Biologie Cellulaires, Université de Poitiers, Poitiers, France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>CNRS-UMR6187, Institut de Physiologie et Biologie Cellulaires, Université de Poitiers, Poitiers</wicri:regionArea><placeName><region type="region">Nouvelle-Aquitaine</region><region type="old region">Poitou-Charentes</region><settlement type="city">Poitiers</settlement></placeName><orgName type="university">Université de Poitiers</orgName></affiliation></author><author><name sortKey="Regnacq, Matthieu" sort="Regnacq, Matthieu" uniqKey="Regnacq M" first="Matthieu" last="Regnacq">Matthieu Regnacq</name></author><author><name sortKey="Colas, Jenny" sort="Colas, Jenny" uniqKey="Colas J" first="Jenny" last="Colas">Jenny Colas</name></author><author><name sortKey="Berges, Thierry" sort="Berges, Thierry" uniqKey="Berges T" first="Thierry" last="Berges">Thierry Berges</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2010">2010</date><idno type="RBID">pubmed:20850523</idno><idno type="pmid">20850523</idno><idno type="doi">10.1016/j.freeradbiomed.2010.09.007</idno><idno type="wicri:Area/PubMed/Corpus">000A25</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000A25</idno><idno type="wicri:Area/PubMed/Curation">000985</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">000985</idno><idno type="wicri:Area/PubMed/Checkpoint">000985</idno><idno type="wicri:explorRef" wicri:stream="Checkpoint" wicri:step="PubMed">000985</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">A Saccharomyces cerevisiae strain unable to store neutral lipids is tolerant to oxidative stress induced by α-synuclein.</title><author><name sortKey="Sere, Yves Y" sort="Sere, Yves Y" uniqKey="Sere Y" first="Yves Y" last="Sere">Yves Y. Sere</name><affiliation wicri:level="4"><nlm:affiliation>CNRS-UMR6187, Institut de Physiologie et Biologie Cellulaires, Université de Poitiers, Poitiers, France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>CNRS-UMR6187, Institut de Physiologie et Biologie Cellulaires, Université de Poitiers, Poitiers</wicri:regionArea><placeName><region type="region">Nouvelle-Aquitaine</region><region type="old region">Poitou-Charentes</region><settlement type="city">Poitiers</settlement></placeName><orgName type="university">Université de Poitiers</orgName></affiliation></author><author><name sortKey="Regnacq, Matthieu" sort="Regnacq, Matthieu" uniqKey="Regnacq M" first="Matthieu" last="Regnacq">Matthieu Regnacq</name></author><author><name sortKey="Colas, Jenny" sort="Colas, Jenny" uniqKey="Colas J" first="Jenny" last="Colas">Jenny Colas</name></author><author><name sortKey="Berges, Thierry" sort="Berges, Thierry" uniqKey="Berges T" first="Thierry" last="Berges">Thierry Berges</name></author></analytic><series><title level="j">Free radical biology & medicine</title><idno type="eISSN">1873-4596</idno><imprint><date when="2010" type="published">2010</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adaptation, Biological (drug effects)</term><term>Adaptation, Biological (genetics)</term><term>Drug Resistance (genetics)</term><term>Enzyme Activation (drug effects)</term><term>Fatty Acid Synthases (metabolism)</term><term>Glutathione (metabolism)</term><term>Lipid Metabolism (genetics)</term><term>Lipid Metabolism Disorders (genetics)</term><term>Lipid Metabolism Disorders (pathology)</term><term>Models, Theoretical</term><term>Organisms, Genetically Modified</term><term>Oxidation-Reduction (drug effects)</term><term>Oxidative Stress (drug effects)</term><term>Oxidative Stress (genetics)</term><term>Oxidative Stress (physiology)</term><term>Saccharomyces cerevisiae (genetics)</term><term>Saccharomyces cerevisiae (growth & development)</term><term>Saccharomyces cerevisiae (metabolism)</term><term>Squalene (metabolism)</term><term>alpha-Synuclein (genetics)</term><term>alpha-Synuclein (metabolism)</term><term>alpha-Synuclein (pharmacology)</term><term>alpha-Synuclein (physiology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>alpha-Synuclein</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Fatty Acid Synthases</term><term>Glutathione</term><term>Squalene</term><term>alpha-Synuclein</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Adaptation, Biological</term><term>Enzyme Activation</term><term>Oxidation-Reduction</term><term>Oxidative Stress</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Adaptation, Biological</term><term>Drug Resistance</term><term>Lipid Metabolism</term><term>Lipid Metabolism Disorders</term><term>Oxidative Stress</term><term>Saccharomyces cerevisiae</term></keywords><keywords scheme="MESH" qualifier="growth & development" xml:lang="en"><term>Saccharomyces cerevisiae</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Saccharomyces cerevisiae</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Lipid Metabolism Disorders</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>alpha-Synuclein</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Oxidative Stress</term><term>alpha-Synuclein</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Models, Theoretical</term><term>Organisms, Genetically Modified</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Parkinson disease is a neurodegenerative pathology that has been linked to several genetic mutations of the SNCA gene encoding the pro-oxidant α-synuclein protein. The budding yeast Saccharomyces cerevisiae is a valuable model for studying the cellular and molecular mechanisms of α-synuclein toxicity. Indeed heterologous expression of α-synuclein is toxic to wild-type yeast and exhibits the main features of damage caused to mammalian neurons, including an increase in neutral lipid storage (triglycerides and steryl esters, embedded into lipid droplets). To address the significance of this accumulation, we forced α-synuclein production in a strain unable to synthesize triglycerides and steryl esters. Surprisingly, the inability to store neutral lipids rendered the cells more tolerant to α-synuclein. Our results indicate that the level of α-synuclein toxicity is correlated with fatty acid synthase activity and intracellular redox status.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">20850523</PMID><DateCreated><Year>2010</Year><Month>11</Month><Day>02</Day></DateCreated><DateCompleted><Year>2011</Year><Month>02</Month><Day>23</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1873-4596</ISSN><JournalIssue CitedMedium="Internet"><Volume>49</Volume><Issue>11</Issue><PubDate><Year>2010</Year><Month>Dec</Month><Day>01</Day></PubDate></JournalIssue><Title>Free radical biology & medicine</Title><ISOAbbreviation>Free Radic. Biol. Med.</ISOAbbreviation></Journal><ArticleTitle>A Saccharomyces cerevisiae strain unable to store neutral lipids is tolerant to oxidative stress induced by α-synuclein.</ArticleTitle><Pagination><MedlinePgn>1755-64</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.freeradbiomed.2010.09.007</ELocationID><Abstract><AbstractText>Parkinson disease is a neurodegenerative pathology that has been linked to several genetic mutations of the SNCA gene encoding the pro-oxidant α-synuclein protein. The budding yeast Saccharomyces cerevisiae is a valuable model for studying the cellular and molecular mechanisms of α-synuclein toxicity. Indeed heterologous expression of α-synuclein is toxic to wild-type yeast and exhibits the main features of damage caused to mammalian neurons, including an increase in neutral lipid storage (triglycerides and steryl esters, embedded into lipid droplets). To address the significance of this accumulation, we forced α-synuclein production in a strain unable to synthesize triglycerides and steryl esters. Surprisingly, the inability to store neutral lipids rendered the cells more tolerant to α-synuclein. Our results indicate that the level of α-synuclein toxicity is correlated with fatty acid synthase activity and intracellular redox status.</AbstractText><CopyrightInformation>Copyright © 2010 Elsevier Inc. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Sere</LastName><ForeName>Yves Y</ForeName><Initials>YY</Initials><AffiliationInfo><Affiliation>CNRS-UMR6187, Institut de Physiologie et Biologie Cellulaires, Université de Poitiers, Poitiers, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Regnacq</LastName><ForeName>Matthieu</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Colas</LastName><ForeName>Jenny</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>Berges</LastName><ForeName>Thierry</ForeName><Initials>T</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2010</Year><Month>09</Month><Day>17</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Free Radic Biol Med</MedlineTA><NlmUniqueID>8709159</NlmUniqueID><ISSNLinking>0891-5849</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D051844">alpha-Synuclein</NameOfSubstance></Chemical><Chemical><RegistryNumber>7QWM220FJH</RegistryNumber><NameOfSubstance UI="D013185">Squalene</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.3.1.85</RegistryNumber><NameOfSubstance UI="D064429">Fatty Acid Synthases</NameOfSubstance></Chemical><Chemical><RegistryNumber>GAN16C9B8O</RegistryNumber><NameOfSubstance UI="D005978">Glutathione</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000220" MajorTopicYN="N">Adaptation, Biological</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug 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MajorTopicYN="Y">physiology</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2010</Year><Month>06</Month><Day>25</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2010</Year><Month>08</Month><Day>27</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2010</Year><Month>09</Month><Day>09</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2010</Year><Month>9</Month><Day>21</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2010</Year><Month>9</Month><Day>21</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2011</Year><Month>2</Month><Day>24</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">20850523</ArticleId><ArticleId IdType="pii">S0891-5849(10)00539-3</ArticleId><ArticleId IdType="doi">10.1016/j.freeradbiomed.2010.09.007</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>France</li></country><region><li>Nouvelle-Aquitaine</li><li>Poitou-Charentes</li></region><settlement><li>Poitiers</li></settlement><orgName><li>Université de Poitiers</li></orgName></list><tree><noCountry><name sortKey="Berges, Thierry" sort="Berges, Thierry" uniqKey="Berges T" first="Thierry" last="Berges">Thierry Berges</name><name sortKey="Colas, Jenny" sort="Colas, Jenny" uniqKey="Colas J" first="Jenny" last="Colas">Jenny Colas</name><name sortKey="Regnacq, Matthieu" sort="Regnacq, Matthieu" uniqKey="Regnacq M" first="Matthieu" last="Regnacq">Matthieu Regnacq</name></noCountry><country name="France"><region name="Nouvelle-Aquitaine"><name sortKey="Sere, Yves Y" sort="Sere, Yves Y" uniqKey="Sere Y" first="Yves Y" last="Sere">Yves Y. 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