CHD8 suppresses p53-mediated apoptosis through histone H1 recruitment during early embryogenesis
The DNA-binding chromodomain helicase CHD8 regulates gene expression but how it acts on specific genes has been unclear. During early embryogenesis in mice, CHD8 recruits histone H1 to the p53-dependent promotors of apoptotic genes and thereby prevents massive cell death at this stage of development...
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| Veröffentlicht in: | Nature cell biology 2009-02, Vol.11 (2), p.172-182 |
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| creator | Nishiyama, Masaaki Oshikawa, Kiyotaka Tsukada, Yu-ichi Nakagawa, Tadashi Iemura, Shun-ichiro Natsume, Tohru Fan, Yuhong Kikuchi, Akira Skoultchi, Arthur I. Nakayama, Keiichi I. |
| description | The DNA-binding chromodomain helicase CHD8 regulates gene expression but how it acts on specific genes has been unclear. During early embryogenesis in mice, CHD8 recruits histone H1 to the p53-dependent promotors of apoptotic genes and thereby prevents massive cell death at this stage of development.
The chromodomain helicase DNA-binding (CHD) family of enzymes is thought to regulate gene expression, but their role in the regulation of specific genes has been unclear. Here we show that CHD8 is expressed at a high level during early embryogenesis and prevents apoptosis mediated by the tumour suppressor protein p53. CHD8 was found to bind to p53 and to suppress its transactivation activity. CHD8 promoted the association of p53 and histone H1, forming a trimeric complex on chromatin that was required for inhibition of p53-dependent transactivation and apoptosis. Depletion of CHD8 or histone H1 resulted in p53 activation and apoptosis. Furthermore,
Chd8
−/−
mice died early during embryogenesis, manifesting widespread apoptosis, whereas deletion of
p53
ameliorated this developmental arrest. These observations reveal a mode of p53 regulation mediated by CHD8, which may set a threshold for induction of apoptosis during early embryogenesis by counteracting p53 function through recruitment of histone H1. |
| doi_str_mv | 10.1038/ncb1831 |
| format | Article |
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The chromodomain helicase DNA-binding (CHD) family of enzymes is thought to regulate gene expression, but their role in the regulation of specific genes has been unclear. Here we show that CHD8 is expressed at a high level during early embryogenesis and prevents apoptosis mediated by the tumour suppressor protein p53. CHD8 was found to bind to p53 and to suppress its transactivation activity. CHD8 promoted the association of p53 and histone H1, forming a trimeric complex on chromatin that was required for inhibition of p53-dependent transactivation and apoptosis. Depletion of CHD8 or histone H1 resulted in p53 activation and apoptosis. Furthermore,
Chd8
−/−
mice died early during embryogenesis, manifesting widespread apoptosis, whereas deletion of
p53
ameliorated this developmental arrest. These observations reveal a mode of p53 regulation mediated by CHD8, which may set a threshold for induction of apoptosis during early embryogenesis by counteracting p53 function through recruitment of histone H1.</description><identifier>ISSN: 1465-7392</identifier><identifier>EISSN: 1476-4679</identifier><identifier>DOI: 10.1038/ncb1831</identifier><identifier>PMID: 19151705</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>Animals ; Apoptosis ; Apoptosis - genetics ; Bioengineering ; Biology ; Biomedical and Life Sciences ; Cadherins - genetics ; Cancer Research ; Cell Biology ; Cell death ; Cell Line ; Cellular proteins ; Deoxyribonucleic acid ; Developmental Biology ; DNA ; DNA methylation ; Down-Regulation - genetics ; Embryonic development ; Embryonic Development - genetics ; Embryonic growth stage ; Embryos ; Enzymes ; Gene Expression Regulation, Developmental - genetics ; Gene mutations ; Genetic aspects ; HeLa Cells ; Histones - genetics ; Humans ; Life Sciences ; Macromolecular Substances - metabolism ; Mice ; Mice, Knockout ; Physiological aspects ; Protein Binding - genetics ; Proteins ; Repressor Proteins - genetics ; Repressor Proteins - metabolism ; Stem Cells ; Tumor Suppressor Protein p53 - genetics</subject><ispartof>Nature cell biology, 2009-02, Vol.11 (2), p.172-182</ispartof><rights>Springer Nature Limited 2009</rights><rights>COPYRIGHT 2009 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group Feb 2009</rights><rights>2009 Macmillan Publishers Limited. All rights reserved. 2009</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c559t-afdef7efb023358ffb11bb26bdb2d6a3760fe8b40caf2c34a047e874daac81aa3</citedby><cites>FETCH-LOGICAL-c559t-afdef7efb023358ffb11bb26bdb2d6a3760fe8b40caf2c34a047e874daac81aa3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/ncb1831$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/ncb1831$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>230,314,776,780,881,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19151705$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Nishiyama, Masaaki</creatorcontrib><creatorcontrib>Oshikawa, Kiyotaka</creatorcontrib><creatorcontrib>Tsukada, Yu-ichi</creatorcontrib><creatorcontrib>Nakagawa, Tadashi</creatorcontrib><creatorcontrib>Iemura, Shun-ichiro</creatorcontrib><creatorcontrib>Natsume, Tohru</creatorcontrib><creatorcontrib>Fan, Yuhong</creatorcontrib><creatorcontrib>Kikuchi, Akira</creatorcontrib><creatorcontrib>Skoultchi, Arthur I.</creatorcontrib><creatorcontrib>Nakayama, Keiichi I.</creatorcontrib><title>CHD8 suppresses p53-mediated apoptosis through histone H1 recruitment during early embryogenesis</title><title>Nature cell biology</title><addtitle>Nat Cell Biol</addtitle><addtitle>Nat Cell Biol</addtitle><description>The DNA-binding chromodomain helicase CHD8 regulates gene expression but how it acts on specific genes has been unclear. During early embryogenesis in mice, CHD8 recruits histone H1 to the p53-dependent promotors of apoptotic genes and thereby prevents massive cell death at this stage of development.
The chromodomain helicase DNA-binding (CHD) family of enzymes is thought to regulate gene expression, but their role in the regulation of specific genes has been unclear. Here we show that CHD8 is expressed at a high level during early embryogenesis and prevents apoptosis mediated by the tumour suppressor protein p53. CHD8 was found to bind to p53 and to suppress its transactivation activity. CHD8 promoted the association of p53 and histone H1, forming a trimeric complex on chromatin that was required for inhibition of p53-dependent transactivation and apoptosis. Depletion of CHD8 or histone H1 resulted in p53 activation and apoptosis. Furthermore,
Chd8
−/−
mice died early during embryogenesis, manifesting widespread apoptosis, whereas deletion of
p53
ameliorated this developmental arrest. These observations reveal a mode of p53 regulation mediated by CHD8, which may set a threshold for induction of apoptosis during early embryogenesis by counteracting p53 function through recruitment of histone H1.</description><subject>Animals</subject><subject>Apoptosis</subject><subject>Apoptosis - genetics</subject><subject>Bioengineering</subject><subject>Biology</subject><subject>Biomedical and Life Sciences</subject><subject>Cadherins - genetics</subject><subject>Cancer Research</subject><subject>Cell Biology</subject><subject>Cell death</subject><subject>Cell Line</subject><subject>Cellular proteins</subject><subject>Deoxyribonucleic acid</subject><subject>Developmental Biology</subject><subject>DNA</subject><subject>DNA methylation</subject><subject>Down-Regulation - genetics</subject><subject>Embryonic development</subject><subject>Embryonic Development - genetics</subject><subject>Embryonic growth stage</subject><subject>Embryos</subject><subject>Enzymes</subject><subject>Gene Expression Regulation, Developmental - genetics</subject><subject>Gene mutations</subject><subject>Genetic aspects</subject><subject>HeLa Cells</subject><subject>Histones - genetics</subject><subject>Humans</subject><subject>Life Sciences</subject><subject>Macromolecular Substances - metabolism</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>Physiological aspects</subject><subject>Protein Binding - genetics</subject><subject>Proteins</subject><subject>Repressor Proteins - genetics</subject><subject>Repressor Proteins - metabolism</subject><subject>Stem Cells</subject><subject>Tumor Suppressor Protein p53 - genetics</subject><issn>1465-7392</issn><issn>1476-4679</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNqFkluL1DAYhoso7rqK_0CKgoeLrjk1SW-EZTzMwoLg4Tqm6ZdOlrbpJqk4_94MM7jOIkguEpLne_Pmy1sUTzE6x4jKt5NpsaT4XnGKmeAV46K5v1vzuhK0ISfFoxivEcKMIfGwOMENrrFA9WnxY7V-L8u4zHOAGCGWc02rETqnE3Slnv2cfHSxTJvgl35TblxMfoJyjcsAJiwujTClsluCm_oSdBi2JYxt2PoeJsiVj4sHVg8Rnhzms-L7xw_fVuvq6vOny9XFVWXqukmVth1YAbZFhNJaWtti3LaEt11LOq6p4MiCbBky2hJDmUZMgBSs09pIrDU9K97tdeelzf5NdhX0oObgRh22ymunjk8mt1G9_6kopqTGPAu8PAgEf7NATGp00cAw6An8EhXnUlIq0X9BggTDosYZfH4HvPZLmHIXFCGEcl7L3bUv9lCvB1Busj67MztFdYEbypAkmGXq_B9UHh2MzuQPsS7vHxW8OSrITIJfqddLjOry65dj9tWeNcHHGMD-6RpGahcvdYhXJp_93eRb7pCnDLzeA3HeBQLC7ZPvav0G4JHYMQ</recordid><startdate>20090201</startdate><enddate>20090201</enddate><creator>Nishiyama, Masaaki</creator><creator>Oshikawa, Kiyotaka</creator><creator>Tsukada, Yu-ichi</creator><creator>Nakagawa, Tadashi</creator><creator>Iemura, Shun-ichiro</creator><creator>Natsume, Tohru</creator><creator>Fan, Yuhong</creator><creator>Kikuchi, Akira</creator><creator>Skoultchi, Arthur I.</creator><creator>Nakayama, Keiichi I.</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><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>ISR</scope><scope>3V.</scope><scope>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7T5</scope><scope>7TK</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20090201</creationdate><title>CHD8 suppresses p53-mediated apoptosis through histone H1 recruitment during early embryogenesis</title><author>Nishiyama, Masaaki ; Oshikawa, Kiyotaka ; Tsukada, Yu-ichi ; Nakagawa, Tadashi ; Iemura, Shun-ichiro ; Natsume, Tohru ; Fan, Yuhong ; Kikuchi, Akira ; Skoultchi, Arthur I. ; Nakayama, Keiichi I.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c559t-afdef7efb023358ffb11bb26bdb2d6a3760fe8b40caf2c34a047e874daac81aa3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Animals</topic><topic>Apoptosis</topic><topic>Apoptosis - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Nature cell biology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Nishiyama, Masaaki</au><au>Oshikawa, Kiyotaka</au><au>Tsukada, Yu-ichi</au><au>Nakagawa, Tadashi</au><au>Iemura, Shun-ichiro</au><au>Natsume, Tohru</au><au>Fan, Yuhong</au><au>Kikuchi, Akira</au><au>Skoultchi, Arthur I.</au><au>Nakayama, Keiichi I.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>CHD8 suppresses p53-mediated apoptosis through histone H1 recruitment during early embryogenesis</atitle><jtitle>Nature cell biology</jtitle><stitle>Nat Cell Biol</stitle><addtitle>Nat Cell Biol</addtitle><date>2009-02-01</date><risdate>2009</risdate><volume>11</volume><issue>2</issue><spage>172</spage><epage>182</epage><pages>172-182</pages><issn>1465-7392</issn><eissn>1476-4679</eissn><abstract>The DNA-binding chromodomain helicase CHD8 regulates gene expression but how it acts on specific genes has been unclear. During early embryogenesis in mice, CHD8 recruits histone H1 to the p53-dependent promotors of apoptotic genes and thereby prevents massive cell death at this stage of development.
The chromodomain helicase DNA-binding (CHD) family of enzymes is thought to regulate gene expression, but their role in the regulation of specific genes has been unclear. Here we show that CHD8 is expressed at a high level during early embryogenesis and prevents apoptosis mediated by the tumour suppressor protein p53. CHD8 was found to bind to p53 and to suppress its transactivation activity. CHD8 promoted the association of p53 and histone H1, forming a trimeric complex on chromatin that was required for inhibition of p53-dependent transactivation and apoptosis. Depletion of CHD8 or histone H1 resulted in p53 activation and apoptosis. Furthermore,
Chd8
−/−
mice died early during embryogenesis, manifesting widespread apoptosis, whereas deletion of
p53
ameliorated this developmental arrest. These observations reveal a mode of p53 regulation mediated by CHD8, which may set a threshold for induction of apoptosis during early embryogenesis by counteracting p53 function through recruitment of histone H1.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>19151705</pmid><doi>10.1038/ncb1831</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Nature cell biology, 2009-02, Vol.11 (2), p.172-182 |
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| source | MEDLINE; SpringerLink Journals; Nature |
| subjects | Animals Apoptosis Apoptosis - genetics Bioengineering Biology Biomedical and Life Sciences Cadherins - genetics Cancer Research Cell Biology Cell death Cell Line Cellular proteins Deoxyribonucleic acid Developmental Biology DNA DNA methylation Down-Regulation - genetics Embryonic development Embryonic Development - genetics Embryonic growth stage Embryos Enzymes Gene Expression Regulation, Developmental - genetics Gene mutations Genetic aspects HeLa Cells Histones - genetics Humans Life Sciences Macromolecular Substances - metabolism Mice Mice, Knockout Physiological aspects Protein Binding - genetics Proteins Repressor Proteins - genetics Repressor Proteins - metabolism Stem Cells Tumor Suppressor Protein p53 - genetics |
| title | CHD8 suppresses p53-mediated apoptosis through histone H1 recruitment during early embryogenesis |
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