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However, it is uncertain whether PRC2 writing of H3K27me3 is mechanistically required for gene silencing. Here, we studied PRC2 function in postnatal mouse cardiomyocytes, where the paucity of cell division obviates bulk H3K27me3 rewriting after each cell cycle. EED (embryonic ectoderm development) inactivation in the postnatal heart (EedCKO) caused lethal dilated cardiomyopathy. Surprisingly, gene upregulation in EedCKO was not coupled with loss of H3K27me3. Rather, the activating histone mark H3K27ac increased. EED interacted with histone deacetylases (HDACs) and enhanced their catalytic activity. HDAC overexpression normalized EedCKO heart function and expression of derepressed genes. Our results uncovered a non-canonical, H3K27me3-independent EED repressive mechanism that is essential for normal heart function. Our results further illustrate that organ dysfunction due to epigenetic dysregulation can be corrected by epigenetic rewiring.<\/jats:p>","DOI":"10.7554\/elife.24570","type":"journal-article","created":{"date-parts":[[2017,4,10]],"date-time":"2017-04-10T08:00:26Z","timestamp":1491811226000},"source":"Crossref","is-referenced-by-count":51,"title":["EED orchestration of heart maturation through interaction with HDACs is H3K27me3-independent"],"prefix":"10.7554","volume":"6","author":[{"given":"Shanshan","family":"Ai","sequence":"first","affiliation":[{"name":"Institute of Molecular Medicine, Peking-Tsinghua Center for Life Sciences, Beijing Key Laboratory of Cardiometabolic Molecular Medicine, Peking University, Beijing, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yong","family":"Peng","sequence":"additional","affiliation":[{"name":"Institute of Molecular Medicine, Peking-Tsinghua Center for Life Sciences, Beijing Key Laboratory of Cardiometabolic Molecular 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