Sch9 regulates ribosome biogenesis via Stb3, Dot6 and Tod6 and the histone deacetylase complex RPD3L.
Identifieur interne : 001264 ( Main/Exploration ); précédent : 001263; suivant : 001265Sch9 regulates ribosome biogenesis via Stb3, Dot6 and Tod6 and the histone deacetylase complex RPD3L.
Auteurs : Alexandre Huber [Suisse] ; Sarah L. French ; Hille Tekotte ; Seda Yerlikaya ; Michael Stahl ; Mariya P. Perepelkina ; Mike Tyers ; Jacques Rougemont ; Ann L. Beyer ; Robbie LoewithSource :
- The EMBO journal [ 1460-2075 ] ; 2011.
Descripteurs français
- KwdFr :
- ARN de transfert (biosynthèse), ARN ribosomique (biosynthèse), Protéines de Saccharomyces cerevisiae (métabolisme), Protéines ribosomiques (biosynthèse), Régulation de l'expression des gènes fongiques (MeSH), Saccharomyces cerevisiae (génétique), Saccharomyces cerevisiae (métabolisme), Transcription génétique (MeSH), Transduction du signal (MeSH).
- MESH :
English descriptors
- KwdEn :
- Gene Expression Regulation, Fungal (MeSH), RNA, Ribosomal (biosynthesis), RNA, Transfer (biosynthesis), Ribosomal Proteins (biosynthesis), Saccharomyces cerevisiae (genetics), Saccharomyces cerevisiae (metabolism), Saccharomyces cerevisiae Proteins (metabolism), Signal Transduction (MeSH), Transcription, Genetic (MeSH).
- MESH :
- chemical , biosynthesis : RNA, Ribosomal, RNA, Transfer, Ribosomal Proteins.
- genetics : Saccharomyces cerevisiae.
- metabolism : Saccharomyces cerevisiae, Saccharomyces cerevisiae Proteins.
- Gene Expression Regulation, Fungal, Signal Transduction, Transcription, Genetic.
Abstract
TORC1 is a conserved multisubunit kinase complex that regulates many aspects of eukaryotic growth including the biosynthesis of ribosomes. The TOR protein kinase resident in TORC1 is responsive to environmental cues and is potently inhibited by the natural product rapamycin. Recent characterization of the rapamycin-sensitive phosphoproteome in yeast has yielded insights into how TORC1 regulates growth. Here, we show that Sch9, an AGC family kinase and direct substrate of TORC1, promotes ribosome biogenesis (Ribi) and ribosomal protein (RP) gene expression via direct inhibitory phosphorylation of the transcriptional repressors Stb3, Dot6 and Tod6. Deletion of STB3, DOT6 and TOD6 partially bypasses the growth and cell size defects of an sch9 strain and reveals interdependent regulation of both Ribi and RP gene expression, and other aspects of Ribi. Dephosphorylation of Stb3, Dot6 and Tod6 enables recruitment of the RPD3L histone deacetylase complex to repress Ribi/RP gene promoters. Taken together with previous studies, these results suggest that Sch9 is a master regulator of ribosome biogenesis through the control of Ribi, RP, ribosomal RNA and tRNA gene transcription.
DOI: 10.1038/emboj.2011.221
PubMed: 21730963
PubMed Central: PMC3160192
Affiliations:
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Le document en format XML
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The TOR protein kinase resident in TORC1 is responsive to environmental cues and is potently inhibited by the natural product rapamycin. Recent characterization of the rapamycin-sensitive phosphoproteome in yeast has yielded insights into how TORC1 regulates growth. Here, we show that Sch9, an AGC family kinase and direct substrate of TORC1, promotes ribosome biogenesis (Ribi) and ribosomal protein (RP) gene expression via direct inhibitory phosphorylation of the transcriptional repressors Stb3, Dot6 and Tod6. Deletion of STB3, DOT6 and TOD6 partially bypasses the growth and cell size defects of an sch9 strain and reveals interdependent regulation of both Ribi and RP gene expression, and other aspects of Ribi. Dephosphorylation of Stb3, Dot6 and Tod6 enables recruitment of the RPD3L histone deacetylase complex to repress Ribi/RP gene promoters. Taken together with previous studies, these results suggest that Sch9 is a master regulator of ribosome biogenesis through the control of Ribi, RP, ribosomal RNA and tRNA gene transcription.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">21730963</PMID><DateCompleted><Year>2011</Year><Month>10</Month><Day>03</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">1460-2075</ISSN><JournalIssue CitedMedium="Internet"><Volume>30</Volume><Issue>15</Issue><PubDate><Year>2011</Year><Month>Jul</Month><Day>05</Day></PubDate></JournalIssue><Title>The EMBO journal</Title><ISOAbbreviation>EMBO J</ISOAbbreviation></Journal><ArticleTitle>Sch9 regulates ribosome biogenesis via Stb3, Dot6 and Tod6 and the histone deacetylase complex RPD3L.</ArticleTitle><Pagination><MedlinePgn>3052-64</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1038/emboj.2011.221</ELocationID><Abstract><AbstractText>TORC1 is a conserved multisubunit kinase complex that regulates many aspects of eukaryotic growth including the biosynthesis of ribosomes. The TOR protein kinase resident in TORC1 is responsive to environmental cues and is potently inhibited by the natural product rapamycin. Recent characterization of the rapamycin-sensitive phosphoproteome in yeast has yielded insights into how TORC1 regulates growth. Here, we show that Sch9, an AGC family kinase and direct substrate of TORC1, promotes ribosome biogenesis (Ribi) and ribosomal protein (RP) gene expression via direct inhibitory phosphorylation of the transcriptional repressors Stb3, Dot6 and Tod6. Deletion of STB3, DOT6 and TOD6 partially bypasses the growth and cell size defects of an sch9 strain and reveals interdependent regulation of both Ribi and RP gene expression, and other aspects of Ribi. Dephosphorylation of Stb3, Dot6 and Tod6 enables recruitment of the RPD3L histone deacetylase complex to repress Ribi/RP gene promoters. Taken together with previous studies, these results suggest that Sch9 is a master regulator of ribosome biogenesis through the control of Ribi, RP, ribosomal RNA and tRNA gene transcription.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Huber</LastName><ForeName>Alexandre</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Department of Molecular Biology and National Center for Competence in Research Program 'Frontiers in Genetics', University of Geneva, Geneva, Switzerland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>French</LastName><ForeName>Sarah L</ForeName><Initials>SL</Initials></Author><Author ValidYN="Y"><LastName>Tekotte</LastName><ForeName>Hille</ForeName><Initials>H</Initials></Author><Author ValidYN="Y"><LastName>Yerlikaya</LastName><ForeName>Seda</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Stahl</LastName><ForeName>Michael</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Perepelkina</LastName><ForeName>Mariya P</ForeName><Initials>MP</Initials></Author><Author ValidYN="Y"><LastName>Tyers</LastName><ForeName>Mike</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Rougemont</LastName><ForeName>Jacques</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>Beyer</LastName><ForeName>Ann L</ForeName><Initials>AL</Initials></Author><Author ValidYN="Y"><LastName>Loewith</LastName><ForeName>Robbie</ForeName><Initials>R</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>206173</GrantID><Agency>European Research Council</Agency><Country>International</Country></Grant><Grant><GrantID>R01 GM063952</GrantID><Acronym>GM</Acronym><Agency>NIGMS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>GM63952</GrantID><Acronym>GM</Acronym><Agency>NIGMS NIH HHS</Agency><Country>United States</Country></Grant><Grant><Agency>Wellcome 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Beyer</name><name sortKey="French, Sarah L" sort="French, Sarah L" uniqKey="French S" first="Sarah L" last="French">Sarah L. French</name><name sortKey="Loewith, Robbie" sort="Loewith, Robbie" uniqKey="Loewith R" first="Robbie" last="Loewith">Robbie Loewith</name><name sortKey="Perepelkina, Mariya P" sort="Perepelkina, Mariya P" uniqKey="Perepelkina M" first="Mariya P" last="Perepelkina">Mariya P. 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