antagonism between dna and h3k27 methylation at the imprinted rasgrf1 locus之间的对抗dna和h3k27印rasgrf1位点甲基化.pdfVIP

Antagonism between DNA and H3K27 Methylation at the Imprinted Rasgrf1 Locus 1. 1. 1 1 1 Anders M. Lindroth , Yoon Jung Park , Chelsea M. McLean , Gregoriy A. Dokshin , Jenna M. Persson , 1,2 3,4 ´ 5 6 6 3,4 Herry Herman , Diego Pasini , Xavier Miro , Mary E. Donohoe , Jeannie T. Lee , Kristian Helin , Paul D. Soloway1* 1 Division of Nutritional Sciences, College of Agriculture and Life Sciences, Cornell University, Ithaca, New York, United States of America, 2 Department of Orthopaedic Surgery, School of Medicine, Padjadjaran State University–Hasan Sadikin General Hospital, Bandung, West Java, Indonesia, 3 Biotech Research and Innovation Centre, University of Copenhagen, Copenhagen, Denmark, 4 Centre for Epigenetics, University of Copenhagen, Copenhagen, Denmark, 5 Department of Molecular Cell Biology, ¨ Max-Planck-Institute of Biophysical Chemistry, Gottingen, Germany, 6 Massachusetts General Hospital, Boston, Massachusetts, United States of America Abstract At the imprinted Rasgrf1 locus in mouse, a cis-acting sequence controls DNA methylation at a differentially methylated domain (DMD). While characterizing epigenetic marks over the DMD, we observed that DNA and H3K27 trimethylation are mutually exclusive, with DNA and H3K27 methylation limited to the paternal and maternal sequences, respectively. The mutual exclusion arises because one mark prevents placement of the other. We demonstrated this in five ways: using 5- azacytidine treatments and mutations at the endo