Extended Data Figure 4: Genome-wide chromatin occupancy reveals EZH1 enrichment at bivalent HSC genes and non-canonical active lymphoid genes.
From: Regulation of embryonic haematopoietic multipotency by EZH1
a, Breakdown of EZH1 binding at promoter regions and associated histone marks. b–d, GO term analysis of EZH1-bound active (b), bivalent (c) and repressed (d) genes. e, Distribution of EZH1-bound genes across the haematopoietic hierarchy (left) and their associated histone marks (right). A, active (H3K4me3-marked); B, bivalent (H3K4me3 and H3K27me3-marked); R, repressed (H3K27me3-marked). f, GSEA analysis of EZH1-bound genes correlated with RNA-seq data upon EZH1 knockdown. g, Sankey diagram showing genome-wide changes in histone methylation status upon EZH1 knockdown. h, Upregulated genes exhibit reciprocal decreases in H3K27me3 levels, as quantified by EpiChIP software. K4, H3K4me3; K27, H3K27me3. See also Fig. 3i. i, Activated (formerly bivalent) HSC genes exhibit increased gene expression upon EZH1 knockdown and loss of H3K27me3. See also Fig. 3j. j, Correlations between changes in H3K27me3 and gene expression levels upon EZH1 knockdown, subdivided by subgroups corresponding to methylation changes. N, null. k, Breakdown of bivalent–bivalent (left), bivalent–repressed (centre) and bivalent–null (right) genes upon EZH1 knockdown across the haematopoietic hierarchy. l, Overlap of EZH1- and EZH2-enriched peaks and the distribution of all EZH1-enriched, EZH2-enriched or common genes across the hierarchy (left), or specifically bivalent genes that become activated upon EZH1 knockdown (middle) and active genes, marked by H3K4me3 in shLUC (right). m, SUZ12 binding (from the ChEA database) across the haematopoietic hierarchy. n, Canonical and non-canonical previously identified targets17 across the haematopoietic hierarchy. o, p, Breakdown of histone marks on non-canonical ProB genes (o) and the genome-wide distribution from CEAS analysis32 (p). q, Changes in actively marked, non-canonical ProB genes (green bar in o), upon EZH1 knockdown. r, SUZ12 and EZH2 binding (ChEA database) at ATAC peaks in Ezh1+/− and Ezh1−/− AGM. *P < 0.05 by one-way ANOVA.
