Transcriptional regulation of FeS biogenesis genes: A possible shield against arsenate toxicity activated by Yap1.
Identifieur interne : 000692 ( Main/Exploration ); précédent : 000691; suivant : 000693Transcriptional regulation of FeS biogenesis genes: A possible shield against arsenate toxicity activated by Yap1.
Auteurs : Sofia M. Da Silva [Portugal] ; Liliana Batista-Nascimento [Allemagne] ; Ana Gaspar-Cordeiro [Portugal] ; Laurence Vernis [France] ; Catarina Pimentel [Portugal] ; Claudina Rodrigues-Pousada [Portugal]Source :
- Biochimica et biophysica acta. General subjects [ 0304-4165 ] ; 2018.
Descripteurs français
- KwdFr :
- Activation de la transcription (effets des médicaments et des substances chimiques), Arséniates (toxicité), Facteurs de transcription (génétique), Facteurs de transcription (métabolisme), Ferrosulfoprotéines (biosynthèse), Ferrosulfoprotéines (effets des médicaments et des substances chimiques), Ferrosulfoprotéines (génétique), Protéines de Saccharomyces cerevisiae (génétique), Protéines de Saccharomyces cerevisiae (métabolisme), Régulation de l'expression des gènes fongiques (effets des médicaments et des substances chimiques), Saccharomyces cerevisiae (croissance et développement), Saccharomyces cerevisiae (effets des médicaments et des substances chimiques), Saccharomyces cerevisiae (génétique), Stress oxydatif (effets des médicaments et des substances chimiques).
- MESH :
- biosynthèse : Ferrosulfoprotéines.
- croissance et développement : Saccharomyces cerevisiae.
- effets des médicaments et des substances chimiques : Activation de la transcription, Ferrosulfoprotéines, Régulation de l'expression des gènes fongiques, Saccharomyces cerevisiae, Stress oxydatif.
- génétique : Facteurs de transcription, Ferrosulfoprotéines, Protéines de Saccharomyces cerevisiae, Saccharomyces cerevisiae.
- métabolisme : Facteurs de transcription, Protéines de Saccharomyces cerevisiae.
- toxicité : Arséniates.
English descriptors
- KwdEn :
- Arsenates (toxicity), Gene Expression Regulation, Fungal (drug effects), Iron-Sulfur Proteins (biosynthesis), Iron-Sulfur Proteins (drug effects), Iron-Sulfur Proteins (genetics), Oxidative Stress (drug effects), Saccharomyces cerevisiae (drug effects), Saccharomyces cerevisiae (genetics), Saccharomyces cerevisiae (growth & development), Saccharomyces cerevisiae Proteins (genetics), Saccharomyces cerevisiae Proteins (metabolism), Transcription Factors (genetics), Transcription Factors (metabolism), Transcriptional Activation (drug effects).
- MESH :
- chemical , biosynthesis : Iron-Sulfur Proteins.
- chemical , drug effects : Iron-Sulfur Proteins.
- chemical , genetics : Iron-Sulfur Proteins, Saccharomyces cerevisiae Proteins, Transcription Factors.
- chemical , metabolism : Saccharomyces cerevisiae Proteins, Transcription Factors.
- chemical , toxicity : Arsenates.
- drug effects : Gene Expression Regulation, Fungal, Oxidative Stress, Saccharomyces cerevisiae, Transcriptional Activation.
- genetics : Saccharomyces cerevisiae.
- growth & development : Saccharomyces cerevisiae.
Abstract
In the eukaryotic model yeast Saccharomyces cerevisiae, arsenic (As) detoxification is regulated by two transcriptional factors, Yap8 and Yap1. Yap8 specifically controls As extrusion from the cell, whether Yap1 avoids arsenic-induced oxidative damages. Accordingly, cells lacking both Yap1 and Yap8 are more sensitive to arsenate than cells lacking each regulator individually. Strikingly enough, the same sensitivity pattern was observed under anoxia, suggesting that Yap1 role in As detoxification might not be restricted to the regulation of the oxidative stress response. This finding prompted us to study the transcriptomic profile of wild-type and yap1 mutant cells exposed to arsenate. Interestingly, we found that, under such conditions, several genes involved in the biogenesis of FeS proteins were upregulated in a Yap1-dependent way. In line with this observation, arsenate treatment decreases the activity of the mitochondrial aconitase, Aco1, an FeS cluster-containing enzyme, this effect being even more pronounced in the yap1 mutant. Reinforcing the relevance of FeS cluster biogenesis in arsenate detoxification, the overexpression of several ISC and CIA machinery genes alleviates the deleterious effect of arsenate caused by the absence of Yap1 and Yap8. Altogether our data suggest that the upregulation of FeS biogenesis genes regulated by Yap1 might work as a cellular shield against arsenate toxicity.
DOI: 10.1016/j.bbagen.2018.07.013
PubMed: 30025855
Affiliations:
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Da Silva</name><affiliation wicri:level="1"><nlm:affiliation>Instituto de Tecnologia Química e Biológica António Xavier, Universidade Nova de Lisboa, Av. da República, 2780-157 Oeiras, Portugal.</nlm:affiliation><country xml:lang="fr">Portugal</country><wicri:regionArea>Instituto de Tecnologia Química e Biológica António Xavier, Universidade Nova de Lisboa, Av. da República, 2780-157 Oeiras</wicri:regionArea><wicri:noRegion>2780-157 Oeiras</wicri:noRegion></affiliation></author><author><name sortKey="Batista Nascimento, Liliana" sort="Batista Nascimento, Liliana" uniqKey="Batista Nascimento L" first="Liliana" last="Batista-Nascimento">Liliana Batista-Nascimento</name><affiliation wicri:level="3"><nlm:affiliation>Instituto de Tecnologia Química e Biológica António Xavier, Universidade Nova de Lisboa, Av. da República, 2780-157 Oeiras, Portugal; Institute of Molecular Biology, 55128 Mainz, Germany.</nlm:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>Instituto de Tecnologia Química e Biológica António Xavier, Universidade Nova de Lisboa, Av. da República, 2780-157 Oeiras, Portugal; Institute of Molecular Biology, 55128 Mainz</wicri:regionArea><placeName><region type="land" nuts="2">Rhénanie-Palatinat</region><settlement type="city">Mayence</settlement></placeName></affiliation></author><author><name sortKey="Gaspar Cordeiro, Ana" sort="Gaspar Cordeiro, Ana" uniqKey="Gaspar Cordeiro A" first="Ana" last="Gaspar-Cordeiro">Ana Gaspar-Cordeiro</name><affiliation wicri:level="1"><nlm:affiliation>Instituto de Tecnologia Química e Biológica António Xavier, Universidade Nova de Lisboa, Av. da República, 2780-157 Oeiras, Portugal.</nlm:affiliation><country xml:lang="fr">Portugal</country><wicri:regionArea>Instituto de Tecnologia Química e Biológica António Xavier, Universidade Nova de Lisboa, Av. da República, 2780-157 Oeiras</wicri:regionArea><wicri:noRegion>2780-157 Oeiras</wicri:noRegion></affiliation></author><author><name sortKey="Vernis, Laurence" sort="Vernis, Laurence" uniqKey="Vernis L" first="Laurence" last="Vernis">Laurence Vernis</name><affiliation wicri:level="3"><nlm:affiliation>CNRS UMR 3348, Centre Universitaire, 91405 Orsay, France; Institut Curie, PSL Research University, UMR 3348, 91405 Orsay, France; Université Paris Sud, Université Paris-Saclay, CNRS UMR3348, 91405 Orsay, France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>CNRS UMR 3348, Centre Universitaire, 91405 Orsay, France; Institut Curie, PSL Research University, UMR 3348, 91405 Orsay, France; Université Paris Sud, Université Paris-Saclay, CNRS UMR3348, 91405 Orsay</wicri:regionArea><placeName><region type="region" nuts="2">Île-de-France</region><settlement type="city">Orsay</settlement></placeName></affiliation></author><author><name sortKey="Pimentel, Catarina" sort="Pimentel, Catarina" uniqKey="Pimentel C" first="Catarina" last="Pimentel">Catarina Pimentel</name><affiliation wicri:level="1"><nlm:affiliation>Instituto de Tecnologia Química e Biológica António Xavier, Universidade Nova de Lisboa, Av. da República, 2780-157 Oeiras, Portugal. 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Electronic address: claudina@itqb.unl.pt.</nlm:affiliation><country xml:lang="fr">Portugal</country><wicri:regionArea>Instituto de Tecnologia Química e Biológica António Xavier, Universidade Nova de Lisboa, Av. da República, 2780-157 Oeiras</wicri:regionArea><wicri:noRegion>2780-157 Oeiras</wicri:noRegion></affiliation></author></analytic><series><title level="j">Biochimica et biophysica acta. General subjects</title><idno type="ISSN">0304-4165</idno><imprint><date when="2018" type="published">2018</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Arsenates (toxicity)</term><term>Gene Expression Regulation, Fungal (drug effects)</term><term>Iron-Sulfur Proteins (biosynthesis)</term><term>Iron-Sulfur Proteins (drug effects)</term><term>Iron-Sulfur Proteins (genetics)</term><term>Oxidative Stress (drug effects)</term><term>Saccharomyces cerevisiae (drug effects)</term><term>Saccharomyces cerevisiae (genetics)</term><term>Saccharomyces cerevisiae (growth & development)</term><term>Saccharomyces cerevisiae Proteins (genetics)</term><term>Saccharomyces cerevisiae Proteins (metabolism)</term><term>Transcription Factors (genetics)</term><term>Transcription Factors (metabolism)</term><term>Transcriptional Activation (drug effects)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Activation de la transcription (effets des médicaments et des substances chimiques)</term><term>Arséniates (toxicité)</term><term>Facteurs de transcription (génétique)</term><term>Facteurs de transcription (métabolisme)</term><term>Ferrosulfoprotéines (biosynthèse)</term><term>Ferrosulfoprotéines (effets des médicaments et des substances chimiques)</term><term>Ferrosulfoprotéines (génétique)</term><term>Protéines de Saccharomyces cerevisiae (génétique)</term><term>Protéines de Saccharomyces cerevisiae (métabolisme)</term><term>Régulation de l'expression des gènes fongiques (effets des médicaments et des substances chimiques)</term><term>Saccharomyces cerevisiae (croissance et développement)</term><term>Saccharomyces cerevisiae (effets des médicaments et des substances chimiques)</term><term>Saccharomyces cerevisiae (génétique)</term><term>Stress oxydatif (effets des médicaments et des substances chimiques)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="biosynthesis" xml:lang="en"><term>Iron-Sulfur Proteins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="drug effects" xml:lang="en"><term>Iron-Sulfur Proteins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Iron-Sulfur Proteins</term><term>Saccharomyces cerevisiae Proteins</term><term>Transcription Factors</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Saccharomyces cerevisiae Proteins</term><term>Transcription Factors</term></keywords><keywords scheme="MESH" type="chemical" qualifier="toxicity" xml:lang="en"><term>Arsenates</term></keywords><keywords scheme="MESH" qualifier="biosynthèse" xml:lang="fr"><term>Ferrosulfoprotéines</term></keywords><keywords scheme="MESH" qualifier="croissance et développement" xml:lang="fr"><term>Saccharomyces cerevisiae</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Gene Expression Regulation, Fungal</term><term>Oxidative Stress</term><term>Saccharomyces cerevisiae</term><term>Transcriptional Activation</term></keywords><keywords scheme="MESH" qualifier="effets des médicaments et des substances chimiques" xml:lang="fr"><term>Activation de la transcription</term><term>Ferrosulfoprotéines</term><term>Régulation de l'expression des gènes fongiques</term><term>Saccharomyces cerevisiae</term><term>Stress oxydatif</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Saccharomyces cerevisiae</term></keywords><keywords scheme="MESH" qualifier="growth & development" xml:lang="en"><term>Saccharomyces cerevisiae</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Facteurs de transcription</term><term>Ferrosulfoprotéines</term><term>Protéines de Saccharomyces cerevisiae</term><term>Saccharomyces cerevisiae</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Facteurs de transcription</term><term>Protéines de Saccharomyces cerevisiae</term></keywords><keywords scheme="MESH" qualifier="toxicité" xml:lang="fr"><term>Arséniates</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">In the eukaryotic model yeast Saccharomyces cerevisiae, arsenic (As) detoxification is regulated by two transcriptional factors, Yap8 and Yap1. Yap8 specifically controls As extrusion from the cell, whether Yap1 avoids arsenic-induced oxidative damages. Accordingly, cells lacking both Yap1 and Yap8 are more sensitive to arsenate than cells lacking each regulator individually. Strikingly enough, the same sensitivity pattern was observed under anoxia, suggesting that Yap1 role in As detoxification might not be restricted to the regulation of the oxidative stress response. This finding prompted us to study the transcriptomic profile of wild-type and yap1 mutant cells exposed to arsenate. Interestingly, we found that, under such conditions, several genes involved in the biogenesis of FeS proteins were upregulated in a Yap1-dependent way. In line with this observation, arsenate treatment decreases the activity of the mitochondrial aconitase, Aco1, an FeS cluster-containing enzyme, this effect being even more pronounced in the yap1 mutant. Reinforcing the relevance of FeS cluster biogenesis in arsenate detoxification, the overexpression of several ISC and CIA machinery genes alleviates the deleterious effect of arsenate caused by the absence of Yap1 and Yap8. Altogether our data suggest that the upregulation of FeS biogenesis genes regulated by Yap1 might work as a cellular shield against arsenate toxicity.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">30025855</PMID><DateCompleted><Year>2019</Year><Month>05</Month><Day>23</Day></DateCompleted><DateRevised><Year>2019</Year><Month>05</Month><Day>23</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Print">0304-4165</ISSN><JournalIssue CitedMedium="Print"><Volume>1862</Volume><Issue>10</Issue><PubDate><Year>2018</Year><Month>10</Month></PubDate></JournalIssue><Title>Biochimica et biophysica acta. General subjects</Title><ISOAbbreviation>Biochim Biophys Acta Gen Subj</ISOAbbreviation></Journal><ArticleTitle>Transcriptional regulation of FeS biogenesis genes: A possible shield against arsenate toxicity activated by Yap1.</ArticleTitle><Pagination><MedlinePgn>2152-2161</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">S0304-4165(18)30204-6</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.bbagen.2018.07.013</ELocationID><Abstract><AbstractText>In the eukaryotic model yeast Saccharomyces cerevisiae, arsenic (As) detoxification is regulated by two transcriptional factors, Yap8 and Yap1. Yap8 specifically controls As extrusion from the cell, whether Yap1 avoids arsenic-induced oxidative damages. Accordingly, cells lacking both Yap1 and Yap8 are more sensitive to arsenate than cells lacking each regulator individually. Strikingly enough, the same sensitivity pattern was observed under anoxia, suggesting that Yap1 role in As detoxification might not be restricted to the regulation of the oxidative stress response. This finding prompted us to study the transcriptomic profile of wild-type and yap1 mutant cells exposed to arsenate. Interestingly, we found that, under such conditions, several genes involved in the biogenesis of FeS proteins were upregulated in a Yap1-dependent way. In line with this observation, arsenate treatment decreases the activity of the mitochondrial aconitase, Aco1, an FeS cluster-containing enzyme, this effect being even more pronounced in the yap1 mutant. Reinforcing the relevance of FeS cluster biogenesis in arsenate detoxification, the overexpression of several ISC and CIA machinery genes alleviates the deleterious effect of arsenate caused by the absence of Yap1 and Yap8. Altogether our data suggest that the upregulation of FeS biogenesis genes regulated by Yap1 might work as a cellular shield against arsenate toxicity.</AbstractText><CopyrightInformation>Copyright © 2018. Published by Elsevier B.V.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>da Silva</LastName><ForeName>Sofia M</ForeName><Initials>SM</Initials><AffiliationInfo><Affiliation>Instituto de Tecnologia Química e Biológica António Xavier, Universidade Nova de Lisboa, Av. da República, 2780-157 Oeiras, Portugal.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Batista-Nascimento</LastName><ForeName>Liliana</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Instituto de Tecnologia Química e Biológica António Xavier, Universidade Nova de Lisboa, Av. da República, 2780-157 Oeiras, Portugal; Institute of Molecular Biology, 55128 Mainz, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Gaspar-Cordeiro</LastName><ForeName>Ana</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Instituto de Tecnologia Química e Biológica António Xavier, Universidade Nova de Lisboa, Av. da República, 2780-157 Oeiras, Portugal.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Vernis</LastName><ForeName>Laurence</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>CNRS UMR 3348, Centre Universitaire, 91405 Orsay, France; Institut Curie, PSL Research University, UMR 3348, 91405 Orsay, France; Université Paris Sud, Université Paris-Saclay, CNRS UMR3348, 91405 Orsay, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Pimentel</LastName><ForeName>Catarina</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Instituto de Tecnologia Química e Biológica António Xavier, Universidade Nova de Lisboa, Av. da República, 2780-157 Oeiras, Portugal. Electronic address: pimentel@itqb.unl.pt.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Rodrigues-Pousada</LastName><ForeName>Claudina</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Instituto de Tecnologia Química e Biológica António Xavier, Universidade Nova de Lisboa, Av. da República, 2780-157 Oeiras, Portugal. Electronic address: claudina@itqb.unl.pt.</Affiliation></AffiliationInfo></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>2018</Year><Month>07</Month><Day>17</Day></ArticleDate></Article><MedlineJournalInfo><Country>Netherlands</Country><MedlineTA>Biochim Biophys Acta Gen Subj</MedlineTA><NlmUniqueID>101731726</NlmUniqueID><ISSNLinking>0304-4165</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D001149">Arsenates</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007506">Iron-Sulfur Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D029701">Saccharomyces cerevisiae Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D014157">Transcription Factors</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C086677">YAP1 protein, S cerevisiae</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D001149" MajorTopicYN="N">Arsenates</DescriptorName><QualifierName UI="Q000633" MajorTopicYN="Y">toxicity</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015966" MajorTopicYN="N">Gene Expression Regulation, Fungal</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007506" MajorTopicYN="N">Iron-Sulfur Proteins</DescriptorName><QualifierName UI="Q000096" MajorTopicYN="Y">biosynthesis</QualifierName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018384" MajorTopicYN="N">Oxidative Stress</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012441" MajorTopicYN="N">Saccharomyces cerevisiae</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000254" MajorTopicYN="N">growth & development</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D029701" MajorTopicYN="N">Saccharomyces cerevisiae Proteins</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014157" MajorTopicYN="N">Transcription Factors</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015533" MajorTopicYN="N">Transcriptional Activation</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">Arsenate</Keyword><Keyword MajorTopicYN="Y">FeS biogenesis</Keyword><Keyword MajorTopicYN="Y">Iron homeostasis</Keyword><Keyword MajorTopicYN="Y">Stress</Keyword><Keyword MajorTopicYN="Y">Yap1</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2018</Year><Month>03</Month><Day>12</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2018</Year><Month>06</Month><Day>22</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2018</Year><Month>07</Month><Day>11</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2018</Year><Month>7</Month><Day>22</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2019</Year><Month>5</Month><Day>24</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2018</Year><Month>7</Month><Day>21</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">30025855</ArticleId><ArticleId IdType="pii">S0304-4165(18)30204-6</ArticleId><ArticleId IdType="doi">10.1016/j.bbagen.2018.07.013</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Allemagne</li><li>France</li><li>Portugal</li></country><region><li>Rhénanie-Palatinat</li><li>Île-de-France</li></region><settlement><li>Mayence</li><li>Orsay</li></settlement></list><tree><country name="Portugal"><noRegion><name sortKey="Da Silva, Sofia M" sort="Da Silva, Sofia M" uniqKey="Da Silva S" first="Sofia M" last="Da Silva">Sofia M. Da Silva</name></noRegion><name sortKey="Gaspar Cordeiro, Ana" sort="Gaspar Cordeiro, Ana" uniqKey="Gaspar Cordeiro A" first="Ana" last="Gaspar-Cordeiro">Ana Gaspar-Cordeiro</name><name sortKey="Pimentel, Catarina" sort="Pimentel, Catarina" uniqKey="Pimentel C" first="Catarina" last="Pimentel">Catarina Pimentel</name><name sortKey="Rodrigues Pousada, Claudina" sort="Rodrigues Pousada, Claudina" uniqKey="Rodrigues Pousada C" first="Claudina" last="Rodrigues-Pousada">Claudina Rodrigues-Pousada</name></country><country name="Allemagne"><region name="Rhénanie-Palatinat"><name sortKey="Batista Nascimento, Liliana" sort="Batista Nascimento, Liliana" uniqKey="Batista Nascimento L" first="Liliana" last="Batista-Nascimento">Liliana Batista-Nascimento</name></region></country><country name="France"><region name="Île-de-France"><name sortKey="Vernis, Laurence" sort="Vernis, Laurence" uniqKey="Vernis L" first="Laurence" last="Vernis">Laurence Vernis</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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