Sin3a-Tet1 interaction activates gene transcription and is required for embryonic stem cell pluripotency
Abstract Sin3a is a core component of histone-deacetylation-activity-associated transcriptional repressor complex, playing important roles in early embryo development. Here, we reported that down-regulation of Sin3a led to the loss of embryonic stem cell (ESC) self-renewal and skewed differentiation...
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| Veröffentlicht in: | Nucleic acids research 2018-07, Vol.46 (12), p.6026-6040 |
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| creator | Zhu, Fugui Zhu, Qianshu Ye, Dan Zhang, Qingquan Yang, Yiwei Guo, Xudong Liu, Zhenping Jiapaer, Zeyidan Wan, Xiaoping Wang, Guiying Chen, Wen Zhu, Songcheng Jiang, Cizhong Shi, Weiyang Kang, Jiuhong |
| description | Abstract
Sin3a is a core component of histone-deacetylation-activity-associated transcriptional repressor complex, playing important roles in early embryo development. Here, we reported that down-regulation of Sin3a led to the loss of embryonic stem cell (ESC) self-renewal and skewed differentiation into mesendoderm lineage. We found that Sin3a functioned as a transcriptional coactivator of the critical Nodal antagonist Lefty1 through interacting with Tet1 to de-methylate the Lefty1 promoter. Further studies showed that two amino acid residues (Phe147, Phe182) in the PAH1 domain of Sin3a are essential for Sin3a-Tet1 interaction and its activity in regulating pluripotency. Furthermore, genome-wide analyses of Sin3a, Tet1 and Pol II ChIP-seq and of 5mC MeDIP-seq revealed that Sin3a acted with Tet1 to facilitate the transcription of a set of their co-target genes. These results link Sin3a to epigenetic DNA modifications in transcriptional activation and have implications for understanding mechanisms underlying versatile functions of Sin3a in mouse ESCs. |
| doi_str_mv | 10.1093/nar/gky347 |
| format | Article |
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Sin3a is a core component of histone-deacetylation-activity-associated transcriptional repressor complex, playing important roles in early embryo development. Here, we reported that down-regulation of Sin3a led to the loss of embryonic stem cell (ESC) self-renewal and skewed differentiation into mesendoderm lineage. We found that Sin3a functioned as a transcriptional coactivator of the critical Nodal antagonist Lefty1 through interacting with Tet1 to de-methylate the Lefty1 promoter. Further studies showed that two amino acid residues (Phe147, Phe182) in the PAH1 domain of Sin3a are essential for Sin3a-Tet1 interaction and its activity in regulating pluripotency. Furthermore, genome-wide analyses of Sin3a, Tet1 and Pol II ChIP-seq and of 5mC MeDIP-seq revealed that Sin3a acted with Tet1 to facilitate the transcription of a set of their co-target genes. These results link Sin3a to epigenetic DNA modifications in transcriptional activation and have implications for understanding mechanisms underlying versatile functions of Sin3a in mouse ESCs.</description><identifier>ISSN: 0305-1048</identifier><identifier>EISSN: 1362-4962</identifier><identifier>DOI: 10.1093/nar/gky347</identifier><identifier>PMID: 29733394</identifier><language>eng</language><publisher>England: Oxford University Press</publisher><subject>Animals ; Cell Differentiation ; Cell Line ; Cell Lineage ; DNA-Binding Proteins - metabolism ; Embryonic Stem Cells - cytology ; Embryonic Stem Cells - metabolism ; Gene regulation, Chromatin and Epigenetics ; Left-Right Determination Factors - genetics ; Left-Right Determination Factors - metabolism ; Mice ; Nodal Protein - metabolism ; Promoter Regions, Genetic ; Protein Interaction Domains and Motifs ; Proto-Oncogene Proteins - metabolism ; Repressor Proteins - chemistry ; Repressor Proteins - genetics ; Repressor Proteins - metabolism ; Transcriptional Activation</subject><ispartof>Nucleic acids research, 2018-07, Vol.46 (12), p.6026-6040</ispartof><rights>The Author(s) 2018. Published by Oxford University Press on behalf of Nucleic Acids Research. 2018</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c408t-d67d311847941eeff8a8e8faa33f91f928776eb56d6f2d3968a6338c9ade1df33</citedby><orcidid>0000-0001-5406-2360 ; 0000-0002-2153-6491</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6158608/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6158608/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,1604,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29733394$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhu, Fugui</creatorcontrib><creatorcontrib>Zhu, Qianshu</creatorcontrib><creatorcontrib>Ye, Dan</creatorcontrib><creatorcontrib>Zhang, Qingquan</creatorcontrib><creatorcontrib>Yang, Yiwei</creatorcontrib><creatorcontrib>Guo, Xudong</creatorcontrib><creatorcontrib>Liu, Zhenping</creatorcontrib><creatorcontrib>Jiapaer, Zeyidan</creatorcontrib><creatorcontrib>Wan, Xiaoping</creatorcontrib><creatorcontrib>Wang, Guiying</creatorcontrib><creatorcontrib>Chen, Wen</creatorcontrib><creatorcontrib>Zhu, Songcheng</creatorcontrib><creatorcontrib>Jiang, Cizhong</creatorcontrib><creatorcontrib>Shi, Weiyang</creatorcontrib><creatorcontrib>Kang, Jiuhong</creatorcontrib><title>Sin3a-Tet1 interaction activates gene transcription and is required for embryonic stem cell pluripotency</title><title>Nucleic acids research</title><addtitle>Nucleic Acids Res</addtitle><description>Abstract
Sin3a is a core component of histone-deacetylation-activity-associated transcriptional repressor complex, playing important roles in early embryo development. Here, we reported that down-regulation of Sin3a led to the loss of embryonic stem cell (ESC) self-renewal and skewed differentiation into mesendoderm lineage. We found that Sin3a functioned as a transcriptional coactivator of the critical Nodal antagonist Lefty1 through interacting with Tet1 to de-methylate the Lefty1 promoter. Further studies showed that two amino acid residues (Phe147, Phe182) in the PAH1 domain of Sin3a are essential for Sin3a-Tet1 interaction and its activity in regulating pluripotency. Furthermore, genome-wide analyses of Sin3a, Tet1 and Pol II ChIP-seq and of 5mC MeDIP-seq revealed that Sin3a acted with Tet1 to facilitate the transcription of a set of their co-target genes. These results link Sin3a to epigenetic DNA modifications in transcriptional activation and have implications for understanding mechanisms underlying versatile functions of Sin3a in mouse ESCs.</description><subject>Animals</subject><subject>Cell Differentiation</subject><subject>Cell Line</subject><subject>Cell Lineage</subject><subject>DNA-Binding Proteins - metabolism</subject><subject>Embryonic Stem Cells - cytology</subject><subject>Embryonic Stem Cells - metabolism</subject><subject>Gene regulation, Chromatin and Epigenetics</subject><subject>Left-Right Determination Factors - genetics</subject><subject>Left-Right Determination Factors - metabolism</subject><subject>Mice</subject><subject>Nodal Protein - metabolism</subject><subject>Promoter Regions, Genetic</subject><subject>Protein Interaction Domains and Motifs</subject><subject>Proto-Oncogene Proteins - metabolism</subject><subject>Repressor Proteins - chemistry</subject><subject>Repressor Proteins - genetics</subject><subject>Repressor Proteins - metabolism</subject><subject>Transcriptional Activation</subject><issn>0305-1048</issn><issn>1362-4962</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>TOX</sourceid><sourceid>EIF</sourceid><recordid>eNp9kcFrFTEQxoNY7LP14h8guQgibJtsstnkIkhprVDwYHsOecnkNbqbbJNs4f337mNr0UsPwxzmN998w4fQe0rOKFHsPJp8vvu9Z7x_hTaUibbhSrSv0YYw0jWUcHmM3pbyixDKacffoONW9YwxxTfo_meIzDS3UCkOsUI2toYU8aE9mgoF7yACrtnEYnOY1mF0OBSc4WEOGRz2KWMYt3mfYrC4VBixhWHA0zAvK6lCtPtTdOTNUODdUz9Bd1eXtxfXzc2Pb98vvt40lhNZGyd6xyiVvFecAngvjQTpjWHMK-pVK_tewLYTTvjWMSWkEYxJq4wD6jxjJ-jLqjvN2xGchbh4H_SUw2jyXicT9P-TGO71Lj1qQTspiFwEPj0J5PQwQ6l6DOXwjomQ5qJbwrp-qU4t6OcVtTmVksE_n6FEH6LRSzR6jWaBP_xr7Bn9m8UCfFyBNE8vCf0ByymbAg</recordid><startdate>20180706</startdate><enddate>20180706</enddate><creator>Zhu, Fugui</creator><creator>Zhu, Qianshu</creator><creator>Ye, Dan</creator><creator>Zhang, Qingquan</creator><creator>Yang, Yiwei</creator><creator>Guo, Xudong</creator><creator>Liu, Zhenping</creator><creator>Jiapaer, Zeyidan</creator><creator>Wan, Xiaoping</creator><creator>Wang, Guiying</creator><creator>Chen, Wen</creator><creator>Zhu, Songcheng</creator><creator>Jiang, Cizhong</creator><creator>Shi, Weiyang</creator><creator>Kang, Jiuhong</creator><general>Oxford University Press</general><scope>TOX</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>5PM</scope><orcidid>https://orcid.org/0000-0001-5406-2360</orcidid><orcidid>https://orcid.org/0000-0002-2153-6491</orcidid></search><sort><creationdate>20180706</creationdate><title>Sin3a-Tet1 interaction activates gene transcription and is required for embryonic stem cell pluripotency</title><author>Zhu, Fugui ; Zhu, Qianshu ; Ye, Dan ; Zhang, Qingquan ; Yang, Yiwei ; Guo, Xudong ; Liu, Zhenping ; Jiapaer, Zeyidan ; Wan, Xiaoping ; Wang, Guiying ; Chen, Wen ; Zhu, Songcheng ; Jiang, Cizhong ; Shi, Weiyang ; Kang, Jiuhong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c408t-d67d311847941eeff8a8e8faa33f91f928776eb56d6f2d3968a6338c9ade1df33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Animals</topic><topic>Cell Differentiation</topic><topic>Cell Line</topic><topic>Cell Lineage</topic><topic>DNA-Binding Proteins - metabolism</topic><topic>Embryonic Stem Cells - cytology</topic><topic>Embryonic Stem Cells - metabolism</topic><topic>Gene regulation, Chromatin and Epigenetics</topic><topic>Left-Right Determination Factors - genetics</topic><topic>Left-Right Determination Factors - metabolism</topic><topic>Mice</topic><topic>Nodal Protein - metabolism</topic><topic>Promoter Regions, Genetic</topic><topic>Protein Interaction Domains and Motifs</topic><topic>Proto-Oncogene Proteins - metabolism</topic><topic>Repressor Proteins - chemistry</topic><topic>Repressor Proteins - genetics</topic><topic>Repressor Proteins - metabolism</topic><topic>Transcriptional Activation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhu, Fugui</creatorcontrib><creatorcontrib>Zhu, Qianshu</creatorcontrib><creatorcontrib>Ye, Dan</creatorcontrib><creatorcontrib>Zhang, Qingquan</creatorcontrib><creatorcontrib>Yang, Yiwei</creatorcontrib><creatorcontrib>Guo, Xudong</creatorcontrib><creatorcontrib>Liu, Zhenping</creatorcontrib><creatorcontrib>Jiapaer, Zeyidan</creatorcontrib><creatorcontrib>Wan, Xiaoping</creatorcontrib><creatorcontrib>Wang, Guiying</creatorcontrib><creatorcontrib>Chen, Wen</creatorcontrib><creatorcontrib>Zhu, Songcheng</creatorcontrib><creatorcontrib>Jiang, Cizhong</creatorcontrib><creatorcontrib>Shi, Weiyang</creatorcontrib><creatorcontrib>Kang, Jiuhong</creatorcontrib><collection>Oxford Journals Open Access Collection</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>PubMed Central (Full Participant titles)</collection><jtitle>Nucleic acids research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhu, Fugui</au><au>Zhu, Qianshu</au><au>Ye, Dan</au><au>Zhang, Qingquan</au><au>Yang, Yiwei</au><au>Guo, Xudong</au><au>Liu, Zhenping</au><au>Jiapaer, Zeyidan</au><au>Wan, Xiaoping</au><au>Wang, Guiying</au><au>Chen, Wen</au><au>Zhu, Songcheng</au><au>Jiang, Cizhong</au><au>Shi, Weiyang</au><au>Kang, Jiuhong</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Sin3a-Tet1 interaction activates gene transcription and is required for embryonic stem cell pluripotency</atitle><jtitle>Nucleic acids research</jtitle><addtitle>Nucleic Acids Res</addtitle><date>2018-07-06</date><risdate>2018</risdate><volume>46</volume><issue>12</issue><spage>6026</spage><epage>6040</epage><pages>6026-6040</pages><issn>0305-1048</issn><eissn>1362-4962</eissn><abstract>Abstract
Sin3a is a core component of histone-deacetylation-activity-associated transcriptional repressor complex, playing important roles in early embryo development. Here, we reported that down-regulation of Sin3a led to the loss of embryonic stem cell (ESC) self-renewal and skewed differentiation into mesendoderm lineage. We found that Sin3a functioned as a transcriptional coactivator of the critical Nodal antagonist Lefty1 through interacting with Tet1 to de-methylate the Lefty1 promoter. Further studies showed that two amino acid residues (Phe147, Phe182) in the PAH1 domain of Sin3a are essential for Sin3a-Tet1 interaction and its activity in regulating pluripotency. Furthermore, genome-wide analyses of Sin3a, Tet1 and Pol II ChIP-seq and of 5mC MeDIP-seq revealed that Sin3a acted with Tet1 to facilitate the transcription of a set of their co-target genes. These results link Sin3a to epigenetic DNA modifications in transcriptional activation and have implications for understanding mechanisms underlying versatile functions of Sin3a in mouse ESCs.</abstract><cop>England</cop><pub>Oxford University Press</pub><pmid>29733394</pmid><doi>10.1093/nar/gky347</doi><tpages>15</tpages><orcidid>https://orcid.org/0000-0001-5406-2360</orcidid><orcidid>https://orcid.org/0000-0002-2153-6491</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Cell Differentiation Cell Line Cell Lineage DNA-Binding Proteins - metabolism Embryonic Stem Cells - cytology Embryonic Stem Cells - metabolism Gene regulation, Chromatin and Epigenetics Left-Right Determination Factors - genetics Left-Right Determination Factors - metabolism Mice Nodal Protein - metabolism Promoter Regions, Genetic Protein Interaction Domains and Motifs Proto-Oncogene Proteins - metabolism Repressor Proteins - chemistry Repressor Proteins - genetics Repressor Proteins - metabolism Transcriptional Activation |
| title | Sin3a-Tet1 interaction activates gene transcription and is required for embryonic stem cell pluripotency |
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