Fig. 6: Loss of H3K9me3 in previously inactive heterochromatin leads to epigenome restructuring.
From: H3K36 Methylation as a Guardian of Epigenome Integrity
a Genome browser tracks of a representative genomic region, demonstrating that in TKO mMSCs, HP1 redistributes to cluster A regions whereas H3K27me3 broadens into cluster B regions. b Heatmaps centered on clusters A and B regions demonstrating a redistribution of HP1 from cluster B to A regions, whereas H3K27me3 broadens from cluster A into B regions following TKO in mMSCs. c Aggregate plots showing increased HP1 signal in expressed genes following TKO in mMSCs. d Genome browser tracks depicting newly accessible regions within cluster B regions in mMSC TKO cells. e Venn diagram comparing the number of ATAC-Seq peaks found in cluster B regions, where 1914 de novo accessible regions appear following TKO in mMSCs. f Genome browser tracks depicting newly accessible regions within cluster B regions following H3K36M-OE in Cal27 cells. g Venn diagram comparing the number of ATAC-Seq peaks found in cluster B regions, where 1008 de novo accessible regions appear following H3K36M-OE in Cal27 cells. h Heatmaps centered on the 1914 new ATAC-Seq peaks opening in mMSC TKO cells, indicating an upregulation of active marks (H3K27ac and H3K4me1) and transcriptional activity. i Heatmaps centered on the 1008 new ATAC-Seq peaks opening in Cal27 H3K36M-OE cells, indicating an upregulation of H3K27ac and transcriptional activity. Normalized signals were either input-normalized (HP1), MS-normalized (for H3K27me3, H3K9me3, H3K27ac and H3K4me1), depth-normalized (ATAC-Seq) or RPKM (reads per kilobase per million mapped) transformed.
