Leo1 is essential for the dynamic regulation of heterochromatin and gene expression during cellular quiescence.
Identifieur interne : 000302 ( Main/Exploration ); précédent : 000301; suivant : 000303Leo1 is essential for the dynamic regulation of heterochromatin and gene expression during cellular quiescence.
Auteurs : Eriko Oya [Suède] ; Mickaël Durand-Dubief [Suède] ; Adiel Cohen [Israël] ; Vladimir Maksimov [Suède] ; Catherine Schurra [France] ; Jun-Ichi Nakayama [Japon] ; Ronit Weisman [Israël] ; Benoit Arcangioli [France] ; Karl Ekwall [Suède]Source :
- Epigenetics & chromatin [ 1756-8935 ] ; 2019.
Descripteurs français
- KwdFr :
- Cycle cellulaire (génétique), Histone (métabolisme), Hétérochromatine (génétique), Hétérochromatine (métabolisme), Phase G0 (génétique), Phase G0 (physiologie), Protéines de Schizosaccharomyces pombe (génétique), Protéines de Schizosaccharomyces pombe (métabolisme), Protéines de liaison à l'ARN (génétique), Protéines de liaison à l'ARN (métabolisme), Protéines nucléaires (métabolisme), RNA polymerase II (génétique), Régulation de l'expression des gènes fongiques (MeSH), Schizosaccharomyces (génétique), Schizosaccharomyces (métabolisme), Épigenèse génétique (MeSH).
- MESH :
- génétique : Cycle cellulaire, Hétérochromatine, Phase G0, Protéines de Schizosaccharomyces pombe, Protéines de liaison à l'ARN, RNA polymerase II, Schizosaccharomyces.
- métabolisme : Histone, Hétérochromatine, Protéines de Schizosaccharomyces pombe, Protéines de liaison à l'ARN, Protéines nucléaires, Schizosaccharomyces.
- physiologie : Phase G0.
- Régulation de l'expression des gènes fongiques, Épigenèse génétique.
English descriptors
- KwdEn :
- Cell Cycle (genetics), Epigenesis, Genetic (MeSH), Gene Expression Regulation, Fungal (MeSH), Heterochromatin (genetics), Heterochromatin (metabolism), Histones (metabolism), Nuclear Proteins (metabolism), RNA Polymerase II (genetics), RNA-Binding Proteins (genetics), RNA-Binding Proteins (metabolism), Resting Phase, Cell Cycle (genetics), Resting Phase, Cell Cycle (physiology), Schizosaccharomyces (genetics), Schizosaccharomyces (metabolism), Schizosaccharomyces pombe Proteins (genetics), Schizosaccharomyces pombe Proteins (metabolism).
- MESH :
- chemical , genetics : Heterochromatin, RNA Polymerase II, RNA-Binding Proteins, Schizosaccharomyces pombe Proteins.
- genetics : Cell Cycle, Resting Phase, Cell Cycle, Schizosaccharomyces.
- chemical , metabolism : Heterochromatin, Histones, Nuclear Proteins, RNA-Binding Proteins, Schizosaccharomyces, Schizosaccharomyces pombe Proteins.
- physiology : Resting Phase, Cell Cycle.
- Epigenesis, Genetic, Gene Expression Regulation, Fungal.
Abstract
BACKGROUND
Cellular quiescence is a reversible differentiation state during which cells modify their gene expression program to inhibit metabolic functions and adapt to a new cellular environment. The epigenetic changes accompanying these alterations are not well understood. We used fission yeast cells as a model to study the regulation of quiescence. When these cells are starved for nitrogen, the cell cycle is arrested in G1, and the cells enter quiescence (G0). A gene regulatory program is initiated, including downregulation of thousands of genes-for example, those related to cell proliferation-and upregulation of specific genes-for example, autophagy genes-needed to adapt to the physiological challenge. These changes in gene expression are accompanied by a marked alteration of nuclear organization and chromatin structure.
RESULTS
Here, we investigated the role of Leo1, a subunit of the conserved RNA polymerase-associated factor 1 (Paf1) complex, in the quiescence process using fission yeast as the model organism. Heterochromatic regions became very dynamic in fission yeast in G0 during nitrogen starvation. The reduction of heterochromatin in early G0 was correlated with reduced target of rapamycin complex 2 (TORC2) signaling. We demonstrated that cells lacking Leo1 show reduced survival in G0. In these cells, heterochromatic regions, including subtelomeres, were stabilized, and the expression of many genes, including membrane transport genes, was abrogated. TOR inhibition mimics the effect of nitrogen starvation, leading to the expression of subtelomeric genes, and this effect was suppressed by genetic deletion of leo1.
CONCLUSIONS
We identified a protein, Leo1, necessary for survival during quiescence. Leo1 is part of a conserved protein complex, Paf1C, linked to RNA polymerase II. We showed that Leo1, acting downstream of TOR, is crucial for the dynamic reorganization of chromosomes and the regulation of gene expression during cellular quiescence. Genes encoding membrane transporters are not expressed in quiescent leo1 mutant cells, and cells die after 2 weeks of nitrogen starvation. Taken together, our results suggest that Leo1 is essential for the dynamic regulation of heterochromatin and gene expression during cellular quiescence.
DOI: 10.1186/s13072-019-0292-7
PubMed: 31315658
PubMed Central: PMC6636030
Affiliations:
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sort="Nakayama, Jun Ichi" uniqKey="Nakayama J" first="Jun-Ichi" last="Nakayama">Jun-Ichi Nakayama</name><affiliation wicri:level="1"><nlm:affiliation>Division of Chromatin Regulation, National Institute for Basic Biology, Okazaki, Japan.</nlm:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Division of Chromatin Regulation, National Institute for Basic Biology, Okazaki</wicri:regionArea><wicri:noRegion>Okazaki</wicri:noRegion></affiliation></author><author><name sortKey="Weisman, Ronit" sort="Weisman, Ronit" uniqKey="Weisman R" first="Ronit" last="Weisman">Ronit Weisman</name><affiliation wicri:level="1"><nlm:affiliation>Department of Natural and Life Sciences, The Open University of Israel, Ra'anana, Israel.</nlm:affiliation><country xml:lang="fr">Israël</country><wicri:regionArea>Department of Natural and Life Sciences, The Open University of Israel, Ra'anana</wicri:regionArea><wicri:noRegion>Ra'anana</wicri:noRegion></affiliation></author><author><name sortKey="Arcangioli, Benoit" sort="Arcangioli, Benoit" uniqKey="Arcangioli B" first="Benoit" last="Arcangioli">Benoit Arcangioli</name><affiliation wicri:level="3"><nlm:affiliation>Unite Dynamique du Génome, Département Génomes et Génétique, Pasteur Institute, Paris, France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>Unite Dynamique du Génome, Département Génomes et Génétique, Pasteur Institute, Paris</wicri:regionArea><placeName><region type="region">Île-de-France</region><region type="old region">Île-de-France</region><settlement type="city">Paris</settlement></placeName></affiliation></author><author><name sortKey="Ekwall, Karl" sort="Ekwall, Karl" uniqKey="Ekwall K" first="Karl" last="Ekwall">Karl Ekwall</name><affiliation wicri:level="1"><nlm:affiliation>Department of Biosciences and Nutrition, Karolinska Institutet, NEO Building, 141 83, Huddinge, Sweden. karl.ekwall@ki.se.</nlm:affiliation><country 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quiescence.</title><author><name sortKey="Oya, Eriko" sort="Oya, Eriko" uniqKey="Oya E" first="Eriko" last="Oya">Eriko Oya</name><affiliation wicri:level="1"><nlm:affiliation>Department of Biosciences and Nutrition, Karolinska Institutet, NEO Building, 141 83, Huddinge, Sweden.</nlm:affiliation><country xml:lang="fr">Suède</country><wicri:regionArea>Department of Biosciences and Nutrition, Karolinska Institutet, NEO Building, 141 83, Huddinge</wicri:regionArea><wicri:noRegion>Huddinge</wicri:noRegion></affiliation></author><author><name sortKey="Durand Dubief, Mickael" sort="Durand Dubief, Mickael" uniqKey="Durand Dubief M" first="Mickaël" last="Durand-Dubief">Mickaël Durand-Dubief</name><affiliation wicri:level="1"><nlm:affiliation>Department of Biosciences and Nutrition, Karolinska Institutet, NEO Building, 141 83, Huddinge, Sweden.</nlm:affiliation><country xml:lang="fr">Suède</country><wicri:regionArea>Department of Biosciences and Nutrition, Karolinska Institutet, NEO Building, 141 83, Huddinge</wicri:regionArea><wicri:noRegion>Huddinge</wicri:noRegion></affiliation></author><author><name sortKey="Cohen, Adiel" sort="Cohen, Adiel" uniqKey="Cohen A" first="Adiel" last="Cohen">Adiel Cohen</name><affiliation wicri:level="1"><nlm:affiliation>Department of Natural and Life Sciences, The Open University of Israel, Ra'anana, Israel.</nlm:affiliation><country xml:lang="fr">Israël</country><wicri:regionArea>Department of Natural and Life Sciences, The Open University of Israel, Ra'anana</wicri:regionArea><wicri:noRegion>Ra'anana</wicri:noRegion></affiliation></author><author><name sortKey="Maksimov, Vladimir" sort="Maksimov, Vladimir" uniqKey="Maksimov V" first="Vladimir" last="Maksimov">Vladimir Maksimov</name><affiliation wicri:level="1"><nlm:affiliation>Department of Biosciences and Nutrition, Karolinska Institutet, NEO Building, 141 83, Huddinge, Sweden.</nlm:affiliation><country xml:lang="fr">Suède</country><wicri:regionArea>Department of Biosciences and Nutrition, Karolinska Institutet, NEO Building, 141 83, Huddinge</wicri:regionArea><wicri:noRegion>Huddinge</wicri:noRegion></affiliation></author><author><name sortKey="Schurra, Catherine" sort="Schurra, Catherine" uniqKey="Schurra C" first="Catherine" last="Schurra">Catherine Schurra</name><affiliation wicri:level="3"><nlm:affiliation>Unite Dynamique du Génome, Département Génomes et Génétique, Pasteur Institute, Paris, France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>Unite Dynamique du Génome, Département Génomes et Génétique, Pasteur Institute, Paris</wicri:regionArea><placeName><region type="region">Île-de-France</region><region type="old region">Île-de-France</region><settlement type="city">Paris</settlement></placeName></affiliation></author><author><name sortKey="Nakayama, Jun Ichi" sort="Nakayama, Jun Ichi" uniqKey="Nakayama J" first="Jun-Ichi" last="Nakayama">Jun-Ichi Nakayama</name><affiliation wicri:level="1"><nlm:affiliation>Division of Chromatin Regulation, National Institute for Basic Biology, Okazaki, Japan.</nlm:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Division of Chromatin Regulation, National Institute for Basic Biology, Okazaki</wicri:regionArea><wicri:noRegion>Okazaki</wicri:noRegion></affiliation></author><author><name sortKey="Weisman, Ronit" sort="Weisman, Ronit" uniqKey="Weisman R" first="Ronit" last="Weisman">Ronit Weisman</name><affiliation wicri:level="1"><nlm:affiliation>Department of Natural and Life Sciences, The Open University of Israel, Ra'anana, Israel.</nlm:affiliation><country xml:lang="fr">Israël</country><wicri:regionArea>Department of Natural and Life Sciences, The Open University of Israel, Ra'anana</wicri:regionArea><wicri:noRegion>Ra'anana</wicri:noRegion></affiliation></author><author><name sortKey="Arcangioli, Benoit" sort="Arcangioli, Benoit" uniqKey="Arcangioli B" first="Benoit" last="Arcangioli">Benoit Arcangioli</name><affiliation wicri:level="3"><nlm:affiliation>Unite Dynamique du Génome, Département Génomes et Génétique, Pasteur Institute, Paris, France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>Unite Dynamique du Génome, Département Génomes et Génétique, Pasteur Institute, Paris</wicri:regionArea><placeName><region type="region">Île-de-France</region><region type="old region">Île-de-France</region><settlement type="city">Paris</settlement></placeName></affiliation></author><author><name sortKey="Ekwall, Karl" sort="Ekwall, Karl" uniqKey="Ekwall K" first="Karl" last="Ekwall">Karl Ekwall</name><affiliation wicri:level="1"><nlm:affiliation>Department of Biosciences and Nutrition, Karolinska Institutet, NEO Building, 141 83, Huddinge, Sweden. karl.ekwall@ki.se.</nlm:affiliation><country xml:lang="fr">Suède</country><wicri:regionArea>Department of Biosciences and Nutrition, Karolinska Institutet, NEO Building, 141 83, Huddinge</wicri:regionArea><wicri:noRegion>Huddinge</wicri:noRegion></affiliation></author></analytic><series><title level="j">Epigenetics & chromatin</title><idno type="eISSN">1756-8935</idno><imprint><date when="2019" type="published">2019</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Cell Cycle (genetics)</term><term>Epigenesis, Genetic (MeSH)</term><term>Gene Expression Regulation, Fungal (MeSH)</term><term>Heterochromatin (genetics)</term><term>Heterochromatin (metabolism)</term><term>Histones (metabolism)</term><term>Nuclear Proteins (metabolism)</term><term>RNA Polymerase II (genetics)</term><term>RNA-Binding Proteins (genetics)</term><term>RNA-Binding Proteins (metabolism)</term><term>Resting Phase, Cell Cycle (genetics)</term><term>Resting Phase, Cell Cycle (physiology)</term><term>Schizosaccharomyces (genetics)</term><term>Schizosaccharomyces (metabolism)</term><term>Schizosaccharomyces pombe Proteins (genetics)</term><term>Schizosaccharomyces pombe Proteins (metabolism)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Cycle cellulaire (génétique)</term><term>Histone (métabolisme)</term><term>Hétérochromatine (génétique)</term><term>Hétérochromatine (métabolisme)</term><term>Phase G0 (génétique)</term><term>Phase G0 (physiologie)</term><term>Protéines de Schizosaccharomyces pombe (génétique)</term><term>Protéines de Schizosaccharomyces pombe (métabolisme)</term><term>Protéines de liaison à l'ARN (génétique)</term><term>Protéines de liaison à l'ARN (métabolisme)</term><term>Protéines nucléaires (métabolisme)</term><term>RNA polymerase II (génétique)</term><term>Régulation de l'expression des gènes fongiques (MeSH)</term><term>Schizosaccharomyces (génétique)</term><term>Schizosaccharomyces (métabolisme)</term><term>Épigenèse génétique (MeSH)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Heterochromatin</term><term>RNA Polymerase II</term><term>RNA-Binding Proteins</term><term>Schizosaccharomyces pombe Proteins</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Cell Cycle</term><term>Resting Phase, Cell Cycle</term><term>Schizosaccharomyces</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Cycle cellulaire</term><term>Hétérochromatine</term><term>Phase G0</term><term>Protéines de Schizosaccharomyces pombe</term><term>Protéines de liaison à l'ARN</term><term>RNA polymerase II</term><term>Schizosaccharomyces</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Heterochromatin</term><term>Histones</term><term>Nuclear Proteins</term><term>RNA-Binding Proteins</term><term>Schizosaccharomyces</term><term>Schizosaccharomyces pombe Proteins</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Histone</term><term>Hétérochromatine</term><term>Protéines de Schizosaccharomyces pombe</term><term>Protéines de liaison à l'ARN</term><term>Protéines nucléaires</term><term>Schizosaccharomyces</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Phase G0</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Resting Phase, Cell Cycle</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Epigenesis, Genetic</term><term>Gene Expression Regulation, Fungal</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Régulation de l'expression des gènes fongiques</term><term>Épigenèse génétique</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p><b>BACKGROUND</b></p><p>Cellular quiescence is a reversible differentiation state during which cells modify their gene expression program to inhibit metabolic functions and adapt to a new cellular environment. The epigenetic changes accompanying these alterations are not well understood. We used fission yeast cells as a model to study the regulation of quiescence. When these cells are starved for nitrogen, the cell cycle is arrested in G1, and the cells enter quiescence (G0). A gene regulatory program is initiated, including downregulation of thousands of genes-for example, those related to cell proliferation-and upregulation of specific genes-for example, autophagy genes-needed to adapt to the physiological challenge. These changes in gene expression are accompanied by a marked alteration of nuclear organization and chromatin structure.</p></div><div type="abstract" xml:lang="en"><p><b>RESULTS</b></p><p>Here, we investigated the role of Leo1, a subunit of the conserved RNA polymerase-associated factor 1 (Paf1) complex, in the quiescence process using fission yeast as the model organism. Heterochromatic regions became very dynamic in fission yeast in G0 during nitrogen starvation. The reduction of heterochromatin in early G0 was correlated with reduced target of rapamycin complex 2 (TORC2) signaling. We demonstrated that cells lacking Leo1 show reduced survival in G0. In these cells, heterochromatic regions, including subtelomeres, were stabilized, and the expression of many genes, including membrane transport genes, was abrogated. TOR inhibition mimics the effect of nitrogen starvation, leading to the expression of subtelomeric genes, and this effect was suppressed by genetic deletion of leo1.</p></div><div type="abstract" xml:lang="en"><p><b>CONCLUSIONS</b></p><p>We identified a protein, Leo1, necessary for survival during quiescence. Leo1 is part of a conserved protein complex, Paf1C, linked to RNA polymerase II. We showed that Leo1, acting downstream of TOR, is crucial for the dynamic reorganization of chromosomes and the regulation of gene expression during cellular quiescence. Genes encoding membrane transporters are not expressed in quiescent leo1 mutant cells, and cells die after 2 weeks of nitrogen starvation. Taken together, our results suggest that Leo1 is essential for the dynamic regulation of heterochromatin and gene expression during cellular quiescence.</p></div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">31315658</PMID><DateCompleted><Year>2020</Year><Month>06</Month><Day>15</Day></DateCompleted><DateRevised><Year>2020</Year><Month>06</Month><Day>15</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">1756-8935</ISSN><JournalIssue CitedMedium="Internet"><Volume>12</Volume><Issue>1</Issue><PubDate><Year>2019</Year><Month>07</Month><Day>17</Day></PubDate></JournalIssue><Title>Epigenetics & chromatin</Title><ISOAbbreviation>Epigenetics Chromatin</ISOAbbreviation></Journal><ArticleTitle>Leo1 is essential for the dynamic regulation of heterochromatin and gene expression during cellular quiescence.</ArticleTitle><Pagination><MedlinePgn>45</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1186/s13072-019-0292-7</ELocationID><Abstract><AbstractText Label="BACKGROUND">Cellular quiescence is a reversible differentiation state during which cells modify their gene expression program to inhibit metabolic functions and adapt to a new cellular environment. The epigenetic changes accompanying these alterations are not well understood. We used fission yeast cells as a model to study the regulation of quiescence. When these cells are starved for nitrogen, the cell cycle is arrested in G1, and the cells enter quiescence (G0). A gene regulatory program is initiated, including downregulation of thousands of genes-for example, those related to cell proliferation-and upregulation of specific genes-for example, autophagy genes-needed to adapt to the physiological challenge. These changes in gene expression are accompanied by a marked alteration of nuclear organization and chromatin structure.</AbstractText><AbstractText Label="RESULTS">Here, we investigated the role of Leo1, a subunit of the conserved RNA polymerase-associated factor 1 (Paf1) complex, in the quiescence process using fission yeast as the model organism. Heterochromatic regions became very dynamic in fission yeast in G0 during nitrogen starvation. The reduction of heterochromatin in early G0 was correlated with reduced target of rapamycin complex 2 (TORC2) signaling. We demonstrated that cells lacking Leo1 show reduced survival in G0. In these cells, heterochromatic regions, including subtelomeres, were stabilized, and the expression of many genes, including membrane transport genes, was abrogated. TOR inhibition mimics the effect of nitrogen starvation, leading to the expression of subtelomeric genes, and this effect was suppressed by genetic deletion of leo1.</AbstractText><AbstractText Label="CONCLUSIONS">We identified a protein, Leo1, necessary for survival during quiescence. Leo1 is part of a conserved protein complex, Paf1C, linked to RNA polymerase II. We showed that Leo1, acting downstream of TOR, is crucial for the dynamic reorganization of chromosomes and the regulation of gene expression during cellular quiescence. Genes encoding membrane transporters are not expressed in quiescent leo1 mutant cells, and cells die after 2 weeks of nitrogen starvation. Taken together, our results suggest that Leo1 is essential for the dynamic regulation of heterochromatin and gene expression during cellular quiescence.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Oya</LastName><ForeName>Eriko</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>Department of Biosciences and Nutrition, Karolinska Institutet, NEO Building, 141 83, Huddinge, Sweden.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Durand-Dubief</LastName><ForeName>Mickaël</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Biosciences and Nutrition, Karolinska Institutet, NEO Building, 141 83, Huddinge, Sweden.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Cohen</LastName><ForeName>Adiel</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Department of Natural and Life Sciences, The Open University of Israel, Ra'anana, Israel.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Maksimov</LastName><ForeName>Vladimir</ForeName><Initials>V</Initials><AffiliationInfo><Affiliation>Department of Biosciences and Nutrition, Karolinska Institutet, NEO Building, 141 83, Huddinge, Sweden.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Schurra</LastName><ForeName>Catherine</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Unite Dynamique du Génome, Département Génomes et Génétique, Pasteur Institute, Paris, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Nakayama</LastName><ForeName>Jun-Ichi</ForeName><Initials>JI</Initials><AffiliationInfo><Affiliation>Division of Chromatin Regulation, National Institute for Basic Biology, Okazaki, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Weisman</LastName><ForeName>Ronit</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Department of Natural and Life Sciences, The Open University of Israel, Ra'anana, Israel.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Arcangioli</LastName><ForeName>Benoit</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>Unite Dynamique du Génome, Département Génomes et Génétique, Pasteur Institute, Paris, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ekwall</LastName><ForeName>Karl</ForeName><Initials>K</Initials><Identifier Source="ORCID">0000-0002-3029-4041</Identifier><AffiliationInfo><Affiliation>Department of Biosciences and Nutrition, Karolinska Institutet, NEO Building, 141 83, Huddinge, Sweden. karl.ekwall@ki.se.</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>2019</Year><Month>07</Month><Day>17</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Epigenetics Chromatin</MedlineTA><NlmUniqueID>101471619</NlmUniqueID><ISSNLinking>1756-8935</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D006570">Heterochromatin</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D006657">Histones</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D009687">Nuclear Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016601">RNA-Binding Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D029702">Schizosaccharomyces pombe Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.7.-</RegistryNumber><NameOfSubstance UI="D012319">RNA Polymerase II</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D002453" MajorTopicYN="N">Cell Cycle</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D044127" MajorTopicYN="N">Epigenesis, Genetic</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015966" MajorTopicYN="N">Gene Expression Regulation, Fungal</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006570" MajorTopicYN="N">Heterochromatin</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006657" MajorTopicYN="N">Histones</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009687" MajorTopicYN="N">Nuclear Proteins</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012319" MajorTopicYN="N">RNA Polymerase II</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016601" MajorTopicYN="N">RNA-Binding Proteins</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016192" MajorTopicYN="N">Resting Phase, Cell Cycle</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012568" MajorTopicYN="N">Schizosaccharomyces</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D029702" MajorTopicYN="N">Schizosaccharomyces pombe Proteins</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">Cellular quiescence</Keyword><Keyword MajorTopicYN="Y">Fission yeast</Keyword><Keyword MajorTopicYN="Y">Gene expression</Keyword><Keyword MajorTopicYN="Y">Heterochromatin</Keyword><Keyword MajorTopicYN="Y">Paf1C</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2019</Year><Month>02</Month><Day>06</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2019</Year><Month>07</Month><Day>10</Day></PubMedPubDate><PubMedPubDate 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Mickael" uniqKey="Durand Dubief M" first="Mickaël" last="Durand-Dubief">Mickaël Durand-Dubief</name><name sortKey="Ekwall, Karl" sort="Ekwall, Karl" uniqKey="Ekwall K" first="Karl" last="Ekwall">Karl Ekwall</name><name sortKey="Maksimov, Vladimir" sort="Maksimov, Vladimir" uniqKey="Maksimov V" first="Vladimir" last="Maksimov">Vladimir Maksimov</name></country><country name="Israël"><noRegion><name sortKey="Cohen, Adiel" sort="Cohen, Adiel" uniqKey="Cohen A" first="Adiel" last="Cohen">Adiel Cohen</name></noRegion><name sortKey="Weisman, Ronit" sort="Weisman, Ronit" uniqKey="Weisman R" first="Ronit" last="Weisman">Ronit Weisman</name></country><country name="France"><region name="Île-de-France"><name sortKey="Schurra, Catherine" sort="Schurra, Catherine" uniqKey="Schurra C" first="Catherine" last="Schurra">Catherine Schurra</name></region><name sortKey="Arcangioli, Benoit" sort="Arcangioli, Benoit" uniqKey="Arcangioli B" first="Benoit" last="Arcangioli">Benoit Arcangioli</name></country><country name="Japon"><noRegion><name sortKey="Nakayama, Jun Ichi" sort="Nakayama, Jun Ichi" uniqKey="Nakayama J" first="Jun-Ichi" last="Nakayama">Jun-Ichi Nakayama</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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