Dynamic DNA methylation orchestrates cardiomyocyte development, maturation and disease
The heart is a highly specialized organ with essential function for the organism throughout life. The significance of DNA methylation in shaping the phenotype of the heart remains only partially known. Here we generate and analyse DNA methylomes from highly purified cardiomyocytes of neonatal, adult...
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| Veröffentlicht in: | Nature communications 2014-10, Vol.5 (1), p.5288, Article 5288 |
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| creator | Gilsbach, Ralf Preissl, Sebastian Grüning, Björn A. Schnick, Tilman Burger, Lukas Benes, Vladimir Würch, Andreas Bönisch, Ulrike Günther, Stefan Backofen, Rolf Fleischmann, Bernd K. Schübeler, Dirk Hein, Lutz |
| description | The heart is a highly specialized organ with essential function for the organism throughout life. The significance of DNA methylation in shaping the phenotype of the heart remains only partially known. Here we generate and analyse DNA methylomes from highly purified cardiomyocytes of neonatal, adult healthy and adult failing hearts. We identify large genomic regions that are differentially methylated during cardiomyocyte development and maturation. Demethylation of cardiomyocyte gene bodies correlates strongly with increased gene expression. Silencing of demethylated genes is characterized by the polycomb mark H3K27me3 or by DNA methylation.
De novo
methylation by DNA methyltransferases 3A/B causes repression of fetal cardiac genes, including essential components of the cardiac sarcomere. Failing cardiomyocytes partially resemble neonatal methylation patterns. This study establishes DNA methylation as a highly dynamic process during postnatal growth of cardiomyocytes and their adaptation to pathological stress in a process tightly linked to gene regulation and activity.
DNA methylation is essential for proper gene expression, development and genome stability. Here the authors present whole-genome DNA methylation analyses of purified mouse cardiomyocytes from newborn, adult and failing hearts and find highly dynamic patterns between the three phenotypes of cardiomyocytes. |
| doi_str_mv | 10.1038/ncomms6288 |
| format | Article |
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De novo
methylation by DNA methyltransferases 3A/B causes repression of fetal cardiac genes, including essential components of the cardiac sarcomere. Failing cardiomyocytes partially resemble neonatal methylation patterns. This study establishes DNA methylation as a highly dynamic process during postnatal growth of cardiomyocytes and their adaptation to pathological stress in a process tightly linked to gene regulation and activity.
DNA methylation is essential for proper gene expression, development and genome stability. Here the authors present whole-genome DNA methylation analyses of purified mouse cardiomyocytes from newborn, adult and failing hearts and find highly dynamic patterns between the three phenotypes of cardiomyocytes.</description><identifier>ISSN: 2041-1723</identifier><identifier>EISSN: 2041-1723</identifier><identifier>DOI: 10.1038/ncomms6288</identifier><identifier>PMID: 25335909</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>13/31 ; 38/15 ; 38/23 ; 38/39 ; 631/136 ; 631/337/176/1988 ; 64/60 ; 692/699/75 ; Animals ; Binding Sites ; Cardiovascular Diseases - metabolism ; Cell Differentiation - genetics ; CpG Islands ; DNA - chemistry ; DNA Methylation ; Echocardiography ; Embryonic Stem Cells - cytology ; Enhancer Elements, Genetic ; Epigenesis, Genetic ; Flow Cytometry ; Gene Expression ; Gene Expression Profiling ; Gene Expression Regulation, Developmental ; Gene Silencing ; Heart - embryology ; Histones - chemistry ; Humanities and Social Sciences ; Humans ; Mice ; multidisciplinary ; Myocytes, Cardiac - metabolism ; Phenotype ; Promoter Regions, Genetic ; Science ; Science (multidisciplinary)</subject><ispartof>Nature communications, 2014-10, Vol.5 (1), p.5288, Article 5288</ispartof><rights>The Author(s) 2014</rights><rights>Copyright Nature Publishing Group Oct 2014</rights><rights>Copyright © 2014, Nature Publishing Group, a division of Macmillan Publishers Limited. All Rights Reserved. 2014 Nature Publishing Group, a division of Macmillan Publishers Limited. All Rights Reserved.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c508t-7fb5a1a58e988537df0f11733e346f7bf94e10f3e7d1a5384fd20ac9d38cc24f3</citedby><cites>FETCH-LOGICAL-c508t-7fb5a1a58e988537df0f11733e346f7bf94e10f3e7d1a5384fd20ac9d38cc24f3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4220495/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4220495/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,41096,42165,51551,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25335909$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Gilsbach, Ralf</creatorcontrib><creatorcontrib>Preissl, Sebastian</creatorcontrib><creatorcontrib>Grüning, Björn A.</creatorcontrib><creatorcontrib>Schnick, Tilman</creatorcontrib><creatorcontrib>Burger, Lukas</creatorcontrib><creatorcontrib>Benes, Vladimir</creatorcontrib><creatorcontrib>Würch, Andreas</creatorcontrib><creatorcontrib>Bönisch, Ulrike</creatorcontrib><creatorcontrib>Günther, Stefan</creatorcontrib><creatorcontrib>Backofen, Rolf</creatorcontrib><creatorcontrib>Fleischmann, Bernd K.</creatorcontrib><creatorcontrib>Schübeler, Dirk</creatorcontrib><creatorcontrib>Hein, Lutz</creatorcontrib><title>Dynamic DNA methylation orchestrates cardiomyocyte development, maturation and disease</title><title>Nature communications</title><addtitle>Nat Commun</addtitle><addtitle>Nat Commun</addtitle><description>The heart is a highly specialized organ with essential function for the organism throughout life. The significance of DNA methylation in shaping the phenotype of the heart remains only partially known. Here we generate and analyse DNA methylomes from highly purified cardiomyocytes of neonatal, adult healthy and adult failing hearts. We identify large genomic regions that are differentially methylated during cardiomyocyte development and maturation. Demethylation of cardiomyocyte gene bodies correlates strongly with increased gene expression. Silencing of demethylated genes is characterized by the polycomb mark H3K27me3 or by DNA methylation.
De novo
methylation by DNA methyltransferases 3A/B causes repression of fetal cardiac genes, including essential components of the cardiac sarcomere. Failing cardiomyocytes partially resemble neonatal methylation patterns. This study establishes DNA methylation as a highly dynamic process during postnatal growth of cardiomyocytes and their adaptation to pathological stress in a process tightly linked to gene regulation and activity.
DNA methylation is essential for proper gene expression, development and genome stability. Here the authors present whole-genome DNA methylation analyses of purified mouse cardiomyocytes from newborn, adult and failing hearts and find highly dynamic patterns between the three phenotypes of cardiomyocytes.</description><subject>13/31</subject><subject>38/15</subject><subject>38/23</subject><subject>38/39</subject><subject>631/136</subject><subject>631/337/176/1988</subject><subject>64/60</subject><subject>692/699/75</subject><subject>Animals</subject><subject>Binding Sites</subject><subject>Cardiovascular Diseases - metabolism</subject><subject>Cell Differentiation - genetics</subject><subject>CpG Islands</subject><subject>DNA - chemistry</subject><subject>DNA Methylation</subject><subject>Echocardiography</subject><subject>Embryonic Stem Cells - cytology</subject><subject>Enhancer Elements, Genetic</subject><subject>Epigenesis, Genetic</subject><subject>Flow Cytometry</subject><subject>Gene Expression</subject><subject>Gene Expression Profiling</subject><subject>Gene Expression Regulation, Developmental</subject><subject>Gene Silencing</subject><subject>Heart - embryology</subject><subject>Histones - chemistry</subject><subject>Humanities and Social Sciences</subject><subject>Humans</subject><subject>Mice</subject><subject>multidisciplinary</subject><subject>Myocytes, Cardiac - metabolism</subject><subject>Phenotype</subject><subject>Promoter Regions, Genetic</subject><subject>Science</subject><subject>Science (multidisciplinary)</subject><issn>2041-1723</issn><issn>2041-1723</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNplkU1LAzEQhoMoVmov_gBZ8KZWk022m70IpfULil7Ua0iTSbul2dRkt7D_3khrrZjLBOaZd96ZQeiM4BuCKb-tlLM2DFLOD9BJihnpkzylh3v_DuqFsMDx0YJwxo5RJ80ozQpcnKCPcVtJW6pk_DJMLNTzdinr0lWJ82oOofayhpAo6XXpbOtUW0OiYQ1Lt7JQ1deJlXXjNyWy0okuA8gAp-jIyGWA3jZ20fvD_dvoqT95fXweDSd9lWFe93MzzSSRGYeC84zm2mBDSE4pUDYw-dQUDAg2FHIdKcqZ0SmWqtCUK5UyQ7vobqO7aqYWtIqWvFyKlS-t9K1wshR_M1U5FzO3FiyN-ymyKHCxFfDus4kDi4VrfBU9CzIgLKeMURKpyw2lvAvBg9l1IFh8n0H8niHC5_uedujP0iNwtQFCTFUz8Hs9_8t9AW1BlSQ</recordid><startdate>20141022</startdate><enddate>20141022</enddate><creator>Gilsbach, Ralf</creator><creator>Preissl, Sebastian</creator><creator>Grüning, Björn A.</creator><creator>Schnick, Tilman</creator><creator>Burger, Lukas</creator><creator>Benes, Vladimir</creator><creator>Würch, Andreas</creator><creator>Bönisch, Ulrike</creator><creator>Günther, Stefan</creator><creator>Backofen, Rolf</creator><creator>Fleischmann, Bernd K.</creator><creator>Schübeler, Dirk</creator><creator>Hein, Lutz</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><general>Nature Pub. 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communications</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Gilsbach, Ralf</au><au>Preissl, Sebastian</au><au>Grüning, Björn A.</au><au>Schnick, Tilman</au><au>Burger, Lukas</au><au>Benes, Vladimir</au><au>Würch, Andreas</au><au>Bönisch, Ulrike</au><au>Günther, Stefan</au><au>Backofen, Rolf</au><au>Fleischmann, Bernd K.</au><au>Schübeler, Dirk</au><au>Hein, Lutz</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Dynamic DNA methylation orchestrates cardiomyocyte development, maturation and disease</atitle><jtitle>Nature communications</jtitle><stitle>Nat Commun</stitle><addtitle>Nat Commun</addtitle><date>2014-10-22</date><risdate>2014</risdate><volume>5</volume><issue>1</issue><spage>5288</spage><pages>5288-</pages><artnum>5288</artnum><issn>2041-1723</issn><eissn>2041-1723</eissn><abstract>The heart is a highly specialized organ with essential function for the organism throughout life. The significance of DNA methylation in shaping the phenotype of the heart remains only partially known. Here we generate and analyse DNA methylomes from highly purified cardiomyocytes of neonatal, adult healthy and adult failing hearts. We identify large genomic regions that are differentially methylated during cardiomyocyte development and maturation. Demethylation of cardiomyocyte gene bodies correlates strongly with increased gene expression. Silencing of demethylated genes is characterized by the polycomb mark H3K27me3 or by DNA methylation.
De novo
methylation by DNA methyltransferases 3A/B causes repression of fetal cardiac genes, including essential components of the cardiac sarcomere. Failing cardiomyocytes partially resemble neonatal methylation patterns. This study establishes DNA methylation as a highly dynamic process during postnatal growth of cardiomyocytes and their adaptation to pathological stress in a process tightly linked to gene regulation and activity.
DNA methylation is essential for proper gene expression, development and genome stability. Here the authors present whole-genome DNA methylation analyses of purified mouse cardiomyocytes from newborn, adult and failing hearts and find highly dynamic patterns between the three phenotypes of cardiomyocytes.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>25335909</pmid><doi>10.1038/ncomms6288</doi><oa>free_for_read</oa></addata></record> |
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| subjects | 13/31 38/15 38/23 38/39 631/136 631/337/176/1988 64/60 692/699/75 Animals Binding Sites Cardiovascular Diseases - metabolism Cell Differentiation - genetics CpG Islands DNA - chemistry DNA Methylation Echocardiography Embryonic Stem Cells - cytology Enhancer Elements, Genetic Epigenesis, Genetic Flow Cytometry Gene Expression Gene Expression Profiling Gene Expression Regulation, Developmental Gene Silencing Heart - embryology Histones - chemistry Humanities and Social Sciences Humans Mice multidisciplinary Myocytes, Cardiac - metabolism Phenotype Promoter Regions, Genetic Science Science (multidisciplinary) |
| title | Dynamic DNA methylation orchestrates cardiomyocyte development, maturation and disease |
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