@Article{Gilsbach_Preissl_Gruning-Dynam_DNA_methy-2014,
  author =	 {Gilsbach, Ralf and Preissl, Sebastian and Gruning, Bjorn A. 
                  and Schnick, Tilman and Burger, Lukas and Benes, Vladimir 
                  and Wurch, Andreas and Bonisch, Ulrike and Gunther, Stefan 
                  and Backofen, Rolf and Fleischmann, Bernd K. and Schubeler, 
                  Dirk and Hein, Lutz},
  title =	 {Dynamic {DNA} methylation orchestrates cardiomyocyte 
                  development, maturation and disease},
  journal =	 {Nat Commun},
  year =	 {2014},
  volume =	 {5},
  number =	 {},
  pages =	 {5288},
  user =	 {kousik},
  pmid =	 {25335909},
  doi = 	 {10.1038/ncomms6288},
  issn = 	 {2041-1723},
  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.}
}