Skip to main content
. 2013 Oct 10;9(1):101–112. doi: 10.4161/epi.26405

Table 2. Chromatin immunoprecipitation in mouse left ventricle shows specific interaction of EZH2 at genes with bi-directional transcription.

     Ink4a, Ink4b, Ak148321/ANRIL
     Pax6, Pax6ost1
     Nppa, Nppa-as1
     Miat, 1700028D13Rik
     α-MHC, β-MHC, AS β-MHC
     Foxd2, 9130206I24Rik
     Hoxc11, Hoxc12, Hotair
     Gata3, 4930412O13Rik
     Dio3, Dio3os
     Ucn, Ucn-as
     Islr2, 1600029o15Rik
     Dll4, Gm14207
     Pou3f3, 2610017I09Rik
     2610100L16Rik, Gm10724
     Hoxa4, Hoxa5, Hoxa6, Hoxa7, 2700086A05Rik
Irx5, 4933436c20Rik
Fbxo44, Fbxo2
     Otx2, Otx2os
     H2-K2, AA388235
     Pcnxl2, Bc021891
     Dlx6, Dlx6as-1
     Tbx2, 2610027K06Rik
     Myl4 (ALC-1), Myl4-AS
     cTn1 (Tnnt3), cTn1-AS
     Tgfβ3, Tgfβ3-AS

Listed are genes as enriched by ChIP using antibodies that recognize EZH2 and H3K27me3 modification.52 Genes on sense and antisense strands are distinguished by an underline. Significant proportion of the genes enriched by EZH2-ChIP in the mouse heart show specific binding of EZH2 at key cardiac genes with antisense RNA expression. Several cardiac genes with antisense RNA expression including the cardiac regulatory lncRNA genes ANRIL, MIAT, and NPPA-AS appear to be bound by EZH2. Genes encoding non-cardiomyocyte expression programs such as the PAX6, which expresses opposite strand transcript is also repressed by direct binding of EZH2 in the heart. Increased expression of Myosin light chain (MYL4) and TGFβ-3 genes was observed in EZH2 deficient mice,10,52 both of which are known to express regulatory antisense transcripts, however, show no direct association of EZH2 at these promoters.52