PRC2 loss of function reshapes the epigenetic landscape of T-ALL. (A) Distribution of H3K27me3 signal in 5-kb regions around the TSS (top); heatmap representing the same distribution (bottom). (B) Distribution of H3K27ac signal in 5-kb regions around the TSS (top); heatmap representing the same distribution (bottom). (C) Global H3K27me3 and H3K27ac ChIP-seq intensities in PRC2 WT or PRC2 ALT primary T-ALL samples. (D) Venn diagram illustrating the overlap between genes with significantly gained H3K27ac and reduced H3K27me3 signal at their promoter in PRC2 ALT T-ALL samples. (E) Bubble plot indicating the enrichment in transcription factors and regulators signatures among the 187-gene set from panel E. (F) Log² fold change in occupancy of H3K27ac at 86 453 individual consensus peaks in T-ALL. The peaks are ranked in order of increasing log² fold change. (G) Global H3K27me3 and H3K27ac ChIP-seq intensities in PRC2 WT primary T-ALL samples upon control or GSK343 3 µM treatment. (H) Venn diagram illustrating the overlap between genes with significantly enriched H3K27ac signal in PRC2 ALT T-ALL and genes significantly gaining H3K27ac signal in PRC2 WT T-ALL upon GSK343. (I) Bar plot indicating the enrichment in transcription factors signatures among the 150-gene set from panel H.