RNF20 Inhibits TFIIS-Facilitated Transcriptional Elongation to Suppress Pro-oncogenic Gene Expression
hBRE1/RNF20 is the major E3 ubiquitin ligase for histone H2B. RNF20 depletion causes a global reduction of monoubiquitylated H2B (H2Bub) levels and augments the expression of growth-promoting, pro-oncogenic genes. Those genes reside preferentially in compact chromatin and are inefficiently transcrib...
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| Veröffentlicht in: | Molecular cell 2011-05, Vol.42 (4), p.477-488 |
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| creator | Shema, Efrat Kim, Jaehoon Roeder, Robert G. Oren, Moshe |
| description | hBRE1/RNF20 is the major E3 ubiquitin ligase for histone H2B. RNF20 depletion causes a global reduction of monoubiquitylated H2B (H2Bub) levels and augments the expression of growth-promoting, pro-oncogenic genes. Those genes reside preferentially in compact chromatin and are inefficiently transcribed under basal conditions. We now report that RNF20, presumably via H2Bub, selectively represses those genes by interfering with chromatin recruitment of TFIIS, a factor capable of relieving stalled RNA polymerase II. RNF20 inhibits the interaction between TFIIS and the PAF1 complex and hinders transcriptional elongation. TFIIS ablation selectively abolishes the upregulation of those genes upon RNF20 depletion and attenuates the cellular response to EGF. Consistent with its positive role in transcription of pro-oncogenic genes, TFIIS expression is elevated in various human tumors. Our findings provide a molecular mechanism for selective gene repression by RNF20 and position TFIIS as a key target of RNF20's tumor suppressor activity.
► RNF20 represses transcription elongation by inhibiting TFIIS binding to chromatin ► Depletion of TFIIS selectively suppresses the activation of pro-oncogenic genes ► TFIIS and RNF20 counter each other in the transcriptional response to EGF ► Excessive TFIIS activity may promote cancer |
| doi_str_mv | 10.1016/j.molcel.2011.03.011 |
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► RNF20 represses transcription elongation by inhibiting TFIIS binding to chromatin ► Depletion of TFIIS selectively suppresses the activation of pro-oncogenic genes ► TFIIS and RNF20 counter each other in the transcriptional response to EGF ► Excessive TFIIS activity may promote cancer</description><identifier>ISSN: 1097-2765</identifier><identifier>EISSN: 1097-4164</identifier><identifier>DOI: 10.1016/j.molcel.2011.03.011</identifier><identifier>PMID: 21596312</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>chromatin ; Chromatin - metabolism ; DNA-directed RNA polymerase ; gene expression ; gene expression regulation ; Gene Expression Regulation, Neoplastic ; genes ; HeLa Cells ; histones ; Histones - genetics ; Histones - metabolism ; Humans ; neoplasms ; Neoplasms - genetics ; Nuclear Proteins - metabolism ; RNA Polymerase II - metabolism ; transcription (genetics) ; Transcription Factors ; Transcription, Genetic ; Transcriptional Elongation Factors - metabolism ; ubiquitin-protein ligase ; Ubiquitin-Protein Ligases - metabolism</subject><ispartof>Molecular cell, 2011-05, Vol.42 (4), p.477-488</ispartof><rights>2011 Elsevier Inc.</rights><rights>Copyright © 2011 Elsevier Inc. All rights reserved.</rights><rights>2011 Elsevier Inc. All rights reserved. 2011</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c584t-17136fe9fd753289a685d923952e8b920230efaaf537e0c03f2c3806a82bb9343</citedby><cites>FETCH-LOGICAL-c584t-17136fe9fd753289a685d923952e8b920230efaaf537e0c03f2c3806a82bb9343</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.molcel.2011.03.011$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>230,315,781,785,886,3551,27929,27930,46000</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21596312$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Shema, Efrat</creatorcontrib><creatorcontrib>Kim, Jaehoon</creatorcontrib><creatorcontrib>Roeder, Robert G.</creatorcontrib><creatorcontrib>Oren, Moshe</creatorcontrib><title>RNF20 Inhibits TFIIS-Facilitated Transcriptional Elongation to Suppress Pro-oncogenic Gene Expression</title><title>Molecular cell</title><addtitle>Mol Cell</addtitle><description>hBRE1/RNF20 is the major E3 ubiquitin ligase for histone H2B. RNF20 depletion causes a global reduction of monoubiquitylated H2B (H2Bub) levels and augments the expression of growth-promoting, pro-oncogenic genes. Those genes reside preferentially in compact chromatin and are inefficiently transcribed under basal conditions. We now report that RNF20, presumably via H2Bub, selectively represses those genes by interfering with chromatin recruitment of TFIIS, a factor capable of relieving stalled RNA polymerase II. RNF20 inhibits the interaction between TFIIS and the PAF1 complex and hinders transcriptional elongation. TFIIS ablation selectively abolishes the upregulation of those genes upon RNF20 depletion and attenuates the cellular response to EGF. Consistent with its positive role in transcription of pro-oncogenic genes, TFIIS expression is elevated in various human tumors. Our findings provide a molecular mechanism for selective gene repression by RNF20 and position TFIIS as a key target of RNF20's tumor suppressor activity.
► RNF20 represses transcription elongation by inhibiting TFIIS binding to chromatin ► Depletion of TFIIS selectively suppresses the activation of pro-oncogenic genes ► TFIIS and RNF20 counter each other in the transcriptional response to EGF ► Excessive TFIIS activity may promote cancer</description><subject>chromatin</subject><subject>Chromatin - metabolism</subject><subject>DNA-directed RNA polymerase</subject><subject>gene expression</subject><subject>gene expression regulation</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>genes</subject><subject>HeLa Cells</subject><subject>histones</subject><subject>Histones - genetics</subject><subject>Histones - metabolism</subject><subject>Humans</subject><subject>neoplasms</subject><subject>Neoplasms - genetics</subject><subject>Nuclear Proteins - metabolism</subject><subject>RNA Polymerase II - metabolism</subject><subject>transcription (genetics)</subject><subject>Transcription Factors</subject><subject>Transcription, Genetic</subject><subject>Transcriptional Elongation Factors - metabolism</subject><subject>ubiquitin-protein ligase</subject><subject>Ubiquitin-Protein Ligases - metabolism</subject><issn>1097-2765</issn><issn>1097-4164</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkUFv1DAQhSMEakvpP0CQG6eEsZ049gUJVbtlpaogdnu2HGey9SprBztb0X9fL7tU7QVOY2u-eZp5L8veEygJEP55U279YHAoKRBSAitTeZWdEZBNURFevT6-acPr0-xtjBsAUtVCnmSnlNSSM0LPMvx5M6eQL9ydbe0U89V8sVgWc23sYCc9YZevgnbRBDtO1js95LPBu7Xef_LJ58vdOAaMMf8RfOGd8Wt01uRX6DCf_f7TSuS77E2vh4gXx3qe3c5nq8tvxfX3q8Xl1-vC1KKaCtIQxnuUfdfUjAqpuag7SZmsKYpWUqAMsNe6r1mDYID11DABXAvatpJV7Dz7ctAdd-0WO4NuCnpQY7BbHR6U11a97Dh7p9b-XjGQEiqZBD4dBYL_tcM4qa2NyeRBO_S7qCQ0hDeCwn9JwQVQLmSTyOpAmuBjDNg_7UNA7aNUG3WIUu2jVMBUKmnsw_Nbnob-ZpeAjweg117pdbBR3S6TAocUNCXkmR2YPL-3GFQ0Fp3BzgY0k-q8_fcOjy7OuyY</recordid><startdate>20110520</startdate><enddate>20110520</enddate><creator>Shema, Efrat</creator><creator>Kim, Jaehoon</creator><creator>Roeder, Robert G.</creator><creator>Oren, Moshe</creator><general>Elsevier Inc</general><scope>6I.</scope><scope>AAFTH</scope><scope>FBQ</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>7TO</scope><scope>8FD</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>RC3</scope><scope>5PM</scope></search><sort><creationdate>20110520</creationdate><title>RNF20 Inhibits TFIIS-Facilitated Transcriptional Elongation to Suppress Pro-oncogenic Gene Expression</title><author>Shema, Efrat ; Kim, Jaehoon ; Roeder, Robert G. ; Oren, Moshe</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c584t-17136fe9fd753289a685d923952e8b920230efaaf537e0c03f2c3806a82bb9343</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>chromatin</topic><topic>Chromatin - metabolism</topic><topic>DNA-directed RNA polymerase</topic><topic>gene expression</topic><topic>gene expression regulation</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>genes</topic><topic>HeLa Cells</topic><topic>histones</topic><topic>Histones - genetics</topic><topic>Histones - metabolism</topic><topic>Humans</topic><topic>neoplasms</topic><topic>Neoplasms - genetics</topic><topic>Nuclear Proteins - metabolism</topic><topic>RNA Polymerase II - metabolism</topic><topic>transcription (genetics)</topic><topic>Transcription Factors</topic><topic>Transcription, Genetic</topic><topic>Transcriptional Elongation Factors - metabolism</topic><topic>ubiquitin-protein ligase</topic><topic>Ubiquitin-Protein Ligases - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Shema, Efrat</creatorcontrib><creatorcontrib>Kim, Jaehoon</creatorcontrib><creatorcontrib>Roeder, Robert G.</creatorcontrib><creatorcontrib>Oren, Moshe</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>AGRIS</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Molecular cell</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Shema, Efrat</au><au>Kim, Jaehoon</au><au>Roeder, Robert G.</au><au>Oren, Moshe</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>RNF20 Inhibits TFIIS-Facilitated Transcriptional Elongation to Suppress Pro-oncogenic Gene Expression</atitle><jtitle>Molecular cell</jtitle><addtitle>Mol Cell</addtitle><date>2011-05-20</date><risdate>2011</risdate><volume>42</volume><issue>4</issue><spage>477</spage><epage>488</epage><pages>477-488</pages><issn>1097-2765</issn><eissn>1097-4164</eissn><abstract>hBRE1/RNF20 is the major E3 ubiquitin ligase for histone H2B. RNF20 depletion causes a global reduction of monoubiquitylated H2B (H2Bub) levels and augments the expression of growth-promoting, pro-oncogenic genes. Those genes reside preferentially in compact chromatin and are inefficiently transcribed under basal conditions. We now report that RNF20, presumably via H2Bub, selectively represses those genes by interfering with chromatin recruitment of TFIIS, a factor capable of relieving stalled RNA polymerase II. RNF20 inhibits the interaction between TFIIS and the PAF1 complex and hinders transcriptional elongation. TFIIS ablation selectively abolishes the upregulation of those genes upon RNF20 depletion and attenuates the cellular response to EGF. Consistent with its positive role in transcription of pro-oncogenic genes, TFIIS expression is elevated in various human tumors. Our findings provide a molecular mechanism for selective gene repression by RNF20 and position TFIIS as a key target of RNF20's tumor suppressor activity.
► RNF20 represses transcription elongation by inhibiting TFIIS binding to chromatin ► Depletion of TFIIS selectively suppresses the activation of pro-oncogenic genes ► TFIIS and RNF20 counter each other in the transcriptional response to EGF ► Excessive TFIIS activity may promote cancer</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>21596312</pmid><doi>10.1016/j.molcel.2011.03.011</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | chromatin Chromatin - metabolism DNA-directed RNA polymerase gene expression gene expression regulation Gene Expression Regulation, Neoplastic genes HeLa Cells histones Histones - genetics Histones - metabolism Humans neoplasms Neoplasms - genetics Nuclear Proteins - metabolism RNA Polymerase II - metabolism transcription (genetics) Transcription Factors Transcription, Genetic Transcriptional Elongation Factors - metabolism ubiquitin-protein ligase Ubiquitin-Protein Ligases - metabolism |
| title | RNF20 Inhibits TFIIS-Facilitated Transcriptional Elongation to Suppress Pro-oncogenic Gene Expression |
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