genome-wide analysis of kap1 binding suggests autoregulation of krab-znfs全基因组分析kap1 krab-znfs绑定显示自动调整.pdfVIP

Genome-Wide Analysis of KAP1 Binding Suggests Autoregulation of KRAB-ZNFs 1,2 1,2 1,2 1,2 3 3 Henriette O’Geen , Sharon L. Squazzo , Sushma Iyengar , Kim Blahnik , John L. Rinn , Howard Y. Chang , Roland 4 1,2* Green , Peggy J. Farnham 1 Department of Pharmacology, University of California Davis, Davis, California, United States of America, 2 The Genome Center, University of California Davis, Davis, California, United States of America, 3 Program in Epithelial Biology, Stanford University School of Medicine, Stanford, California, United States of America, 4 NimbleGen Systems, Madison, Wisconsin, United States of America We performed a genome-scale chromatin immunoprecipitation (ChIP)-chip comparison of two modifications (trimethylation of lysine 9 [H3me3K9] and trimethylation of lysine 27 [H3me3K27]) of histone H3 in Ntera2 testicular carcinoma cells and in three different anatomical sources of primary human fibroblasts. We found that in each of the cell types the two modifications were differentially enriched at the promoters of the two largest classes of transcription factors. Specifically, zinc finger (ZNF) genes were bound by H3me3K9 and homeobox genes were bound by H3me3K27. We have previously shown that the Polycomb repressive complex 2 is responsible for mediating trimethylation of lysine 27 of histone H3 in human cancer cells. In contrast, there is little overlap between H3me3K9 targets and components of the Polycomb repressive complex 2, suggesting that a different histone methyltransferase is responsible for the H3me3K9 modification. Previous studies have shown that SETDB1 can trimethylate H3 on