Fig. 3
EZH2 inhibition does not completely mimic H3K27M effects and EZH2-Y641N partly overcomes H3K27M-induced effects (a, b). Changes in H3K27me2/3 levels and distribution upon EZH2 inhibition. a Example ChIP-seq tracks of H3K27me2/3 distribution in G477 (wild-type) and BT245 (H3K27M) cell lines treated and not treated with UNC1999 (EZH1/2 inhibitor), ChIP-Rx normalized. For comparison, G477 cell line with H3.3-K27M overexpression is also included. b Heatmap plots of ChIP-seq signal intensity for H3K27me2 and H3K27me3 over CGIs for G477 cell line (wild-type) treated and not treated with UNC1999, as well as with H3.3-K27M overexpression. CGIs are separated by kmeans clustering (k = 3). c–e Changes in H3K27me2/3 levels and distribution upon overexpression of EZH2-wt and EZH2-Y641N. c Example ChIP-seq tracks (ChIP-Rx normalized) of H3K27me2/3 distribution in BT245 cell line (H3K27M) overexpressing wild-type or Y641N mutant forms of EZH2. Parental BT245 and CRISPR-edited K27M-KO clone are included for comparison. d Average enrichment at the top 1% of 1 kb bins for H3K27me3. e Proportion of H3K27me3 reads in CGIs and promoters upon EZH2 overexpression. Source data are provided as a Source Data file
