Extended Data Fig. 6: PRC2 hyperactivity leads to H3K27me3 spreading on chromatin.
From: Drug addiction unveils a repressive methylation ceiling in EZH2-mutant lymphoma
a, Aggregate profile plots of Karpas-422 ENCODE ChIP-seq signal (y-axis) for the specified histone modifications centered around gene bodies (x-axis). b, Aggregate profile plots of Karpas-422 H3K27me3 ChIP-Rx signal (y-axis, left) and log2(fold-change) H3K27me3 ChIP-Rx signal relative to GSK343-treated CXCdel+/– cells (y-axis, right) centered around H3K36me3 domains in wild-type cells (x-axis). c, Density plot depicting the distribution of H3K27me3 ChIP-Rx signal (x-axis) of K562 wild-type and CXCdel+/+/+ cells for 50-kb genomic bins. d, Line plot depicting cumulative fraction H3K27me3 ChIP-seq coverage relative to that of the bin with the highest coverage (y-axis) as a function of the region’s relative genomic rank (x-axis) for K562 wild-type and CXCdel+/+/+ cells. e, Same as b. but for K562. f, Density plot depicting EZH2 ChIP-seq signal rank for vehicle-treated Karpas-422 wild-type cells (y-axis) relative to H3K27me3 ChIP-Rx signal rank for vehicle-treated wild-type cells (x-axis, left) and EZH2 ChIP-seq signal rank for vehicle-treated CXCdel+/– (x-axis, right). g, Same as f. but for K562. Results in b-c,e-g represent average of two biological replicates.
