DNA damage regulates direct association of TOR kinase with the RNA polymerase II-transcribed HMO1 gene.
Identifieur interne : 000881 ( Main/Exploration ); précédent : 000880; suivant : 000882DNA damage regulates direct association of TOR kinase with the RNA polymerase II-transcribed HMO1 gene.
Auteurs : Arvind Panday [États-Unis] ; Ashish Gupta [États-Unis] ; Kavitha Srinivasa [États-Unis] ; Lijuan Xiao [États-Unis] ; Mathew D. Smith [États-Unis] ; Anne Grove [États-Unis]Source :
- Molecular biology of the cell [ 1939-4586 ] ; 2017.
Descripteurs français
- KwdFr :
- ARN ribosomique (métabolisme), Cassures double-brin de l'ADN (MeSH), Facteurs de transcription (métabolisme), Protéines HMG (génétique), Protéines HMG (métabolisme), Protéines de Saccharomyces cerevisiae (génétique), Protéines de Saccharomyces cerevisiae (métabolisme), Protéines de liaison à l'ADN (métabolisme), Protéines ribosomiques (métabolisme), RNA polymerase I (génétique), RNA polymerase II (métabolisme), Régions promotrices (génétique) (MeSH), Régulation de l'expression des gènes fongiques (MeSH), Régulation négative (MeSH), Saccharomyces cerevisiae (MeSH), Sérine-thréonine kinases TOR (métabolisme), Transcription génétique (MeSH), Transduction du signal (MeSH).
- MESH :
- génétique : Protéines HMG, Protéines de Saccharomyces cerevisiae, RNA polymerase I.
- métabolisme : ARN ribosomique, Facteurs de transcription, Protéines HMG, Protéines de Saccharomyces cerevisiae, Protéines de liaison à l'ADN, Protéines ribosomiques, RNA polymerase II, Sérine-thréonine kinases TOR.
- Cassures double-brin de l'ADN, Régions promotrices (génétique), Régulation de l'expression des gènes fongiques, Régulation négative, Saccharomyces cerevisiae, Transcription génétique, Transduction du signal.
English descriptors
- KwdEn :
- DNA Breaks, Double-Stranded (MeSH), DNA-Binding Proteins (metabolism), Down-Regulation (MeSH), Gene Expression Regulation, Fungal (MeSH), High Mobility Group Proteins (genetics), High Mobility Group Proteins (metabolism), Promoter Regions, Genetic (MeSH), RNA Polymerase I (genetics), RNA Polymerase II (metabolism), RNA, Ribosomal (metabolism), Ribosomal Proteins (metabolism), Saccharomyces cerevisiae (MeSH), Saccharomyces cerevisiae Proteins (genetics), Saccharomyces cerevisiae Proteins (metabolism), Signal Transduction (MeSH), TOR Serine-Threonine Kinases (metabolism), Transcription Factors (metabolism), Transcription, Genetic (MeSH).
- MESH :
- chemical , genetics : High Mobility Group Proteins, RNA Polymerase I, Saccharomyces cerevisiae Proteins.
- chemical , metabolism : DNA-Binding Proteins, High Mobility Group Proteins, RNA Polymerase II, RNA, Ribosomal, Ribosomal Proteins, Saccharomyces cerevisiae Proteins, TOR Serine-Threonine Kinases, Transcription Factors.
- DNA Breaks, Double-Stranded, Down-Regulation, Gene Expression Regulation, Fungal, Promoter Regions, Genetic, Saccharomyces cerevisiae, Signal Transduction, Transcription, Genetic.
Abstract
The mechanistic target of rapamycin complex 1 (mTORC1) senses nutrient sufficiency and cellular stress. When mTORC1 is inhibited, protein synthesis is reduced in an intricate process that includes a concerted down-regulation of genes encoding rRNA and ribosomal proteins. The Saccharomyces cerevisiae high-mobility group protein Hmo1p has been implicated in coordinating this response to mTORC1 inhibition. We show here that Tor1p binds directly to the HMO1 gene (but not to genes that are not linked to ribosome biogenesis) and that the presence of Tor1p is associated with activation of gene activity. Persistent induction of DNA double-strand breaks or mTORC1 inhibition by rapamycin results in reduced levels of HMO1 mRNA, but only in the presence of Tor1p. This down-regulation is accompanied by eviction of Ifh1p and recruitment of Crf1p, followed by concerted dissociation of Hmo1p and Tor1p. These findings uncover a novel role for TOR kinase in control of gene activity by direct association with an RNA polymerase II-transcribed gene.
DOI: 10.1091/mbc.E17-01-0024
PubMed: 28701348
PubMed Central: PMC5576907
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
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When mTORC1 is inhibited, protein synthesis is reduced in an intricate process that includes a concerted down-regulation of genes encoding rRNA and ribosomal proteins. The <i>Saccharomyces cerevisiae</i> high-mobility group protein Hmo1p has been implicated in coordinating this response to mTORC1 inhibition. We show here that Tor1p binds directly to the <i>HMO1</i> gene (but not to genes that are not linked to ribosome biogenesis) and that the presence of Tor1p is associated with activation of gene activity. Persistent induction of DNA double-strand breaks or mTORC1 inhibition by rapamycin results in reduced levels of <i>HMO1</i> mRNA, but only in the presence of Tor1p. This down-regulation is accompanied by eviction of Ifh1p and recruitment of Crf1p, followed by concerted dissociation of Hmo1p and Tor1p. These findings uncover a novel role for TOR kinase in control of gene activity by direct association with an RNA polymerase II-transcribed gene.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">28701348</PMID><DateCompleted><Year>2017</Year><Month>11</Month><Day>16</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1939-4586</ISSN><JournalIssue CitedMedium="Internet"><Volume>28</Volume><Issue>18</Issue><PubDate><Year>2017</Year><Month>Sep</Month><Day>01</Day></PubDate></JournalIssue><Title>Molecular biology of the cell</Title><ISOAbbreviation>Mol Biol Cell</ISOAbbreviation></Journal><ArticleTitle>DNA damage regulates direct association of TOR kinase with the RNA polymerase II-transcribed <i>HMO1</i> gene.</ArticleTitle><Pagination><MedlinePgn>2449-2459</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1091/mbc.E17-01-0024</ELocationID><Abstract><AbstractText>The mechanistic target of rapamycin complex 1 (mTORC1) senses nutrient sufficiency and cellular stress. When mTORC1 is inhibited, protein synthesis is reduced in an intricate process that includes a concerted down-regulation of genes encoding rRNA and ribosomal proteins. The <i>Saccharomyces cerevisiae</i> high-mobility group protein Hmo1p has been implicated in coordinating this response to mTORC1 inhibition. We show here that Tor1p binds directly to the <i>HMO1</i> gene (but not to genes that are not linked to ribosome biogenesis) and that the presence of Tor1p is associated with activation of gene activity. Persistent induction of DNA double-strand breaks or mTORC1 inhibition by rapamycin results in reduced levels of <i>HMO1</i> mRNA, but only in the presence of Tor1p. This down-regulation is accompanied by eviction of Ifh1p and recruitment of Crf1p, followed by concerted dissociation of Hmo1p and Tor1p. These findings uncover a novel role for TOR kinase in control of gene activity by direct association with an RNA polymerase II-transcribed gene.</AbstractText><CopyrightInformation>© 2017 Panday et al. This article is distributed by The American Society for Cell Biology under license from the author(s). Two months after publication it is available to the public under an Attribution–Noncommercial–Share Alike 3.0 Unported Creative Commons License (http://creativecommons.org/licenses/by-nc-sa/3.0).</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Panday</LastName><ForeName>Arvind</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Department of Biological Sciences, Louisiana State University, Baton Rouge, LA 70803.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Gupta</LastName><ForeName>Ashish</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Department of Biological Sciences, Louisiana State University, Baton Rouge, LA 70803.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Srinivasa</LastName><ForeName>Kavitha</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>Department of Biological Sciences, Louisiana State University, Baton Rouge, LA 70803.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Xiao</LastName><ForeName>Lijuan</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Department of Biological Sciences, Louisiana State University, Baton Rouge, LA 70803.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Smith</LastName><ForeName>Mathew D</ForeName><Initials>MD</Initials><AffiliationInfo><Affiliation>Department of Biological Sciences, Louisiana State University, Baton Rouge, LA 70803.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Grove</LastName><ForeName>Anne</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Department of Biological Sciences, Louisiana State University, Baton Rouge, LA 70803 agrove@lsu.edu.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2017</Year><Month>07</Month><Day>12</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Mol Biol Cell</MedlineTA><NlmUniqueID>9201390</NlmUniqueID><ISSNLinking>1059-1524</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D004268">DNA-Binding Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C103154">HMO1 protein, S cerevisiae</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D006609">High Mobility Group Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D012335">RNA, Ribosomal</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D012269">Ribosomal 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>EC 2.7.1.1</RegistryNumber><NameOfSubstance UI="D058570">TOR Serine-Threonine Kinases</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.7.-</RegistryNumber><NameOfSubstance UI="D012319">RNA Polymerase II</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.7.6</RegistryNumber><NameOfSubstance UI="D012318">RNA Polymerase I</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D053903" MajorTopicYN="Y">DNA Breaks, Double-Stranded</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004268" MajorTopicYN="N">DNA-Binding Proteins</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015536" MajorTopicYN="N">Down-Regulation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015966" MajorTopicYN="N">Gene Expression Regulation, Fungal</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006609" MajorTopicYN="N">High Mobility Group Proteins</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011401" MajorTopicYN="N">Promoter Regions, Genetic</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012318" MajorTopicYN="N">RNA Polymerase I</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012319" MajorTopicYN="N">RNA Polymerase II</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012335" MajorTopicYN="N">RNA, Ribosomal</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012269" MajorTopicYN="N">Ribosomal Proteins</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012441" MajorTopicYN="N">Saccharomyces cerevisiae</DescriptorName></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="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D058570" MajorTopicYN="N">TOR Serine-Threonine Kinases</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014157" MajorTopicYN="N">Transcription Factors</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014158" MajorTopicYN="N">Transcription, Genetic</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2017</Year><Month>01</Month><Day>12</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2017</Year><Month>06</Month><Day>05</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2017</Year><Month>07</Month><Day>07</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2017</Year><Month>7</Month><Day>14</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2017</Year><Month>11</Month><Day>29</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate 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last="Panday">Arvind Panday</name></region><name sortKey="Grove, Anne" sort="Grove, Anne" uniqKey="Grove A" first="Anne" last="Grove">Anne Grove</name><name sortKey="Gupta, Ashish" sort="Gupta, Ashish" uniqKey="Gupta A" first="Ashish" last="Gupta">Ashish Gupta</name><name sortKey="Smith, Mathew D" sort="Smith, Mathew D" uniqKey="Smith M" first="Mathew D" last="Smith">Mathew D. Smith</name><name sortKey="Srinivasa, Kavitha" sort="Srinivasa, Kavitha" uniqKey="Srinivasa K" first="Kavitha" last="Srinivasa">Kavitha Srinivasa</name><name sortKey="Xiao, Lijuan" sort="Xiao, Lijuan" uniqKey="Xiao L" first="Lijuan" last="Xiao">Lijuan Xiao</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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