Effects of genome-wide binding of WT versus mutant ASXL1 on histone modifications. (A) Overlap of Asxl1- and FLAG-binding sites in c-Kit⁺ control cells and KI cells. Asxl1 antibody recognizes the N terminus of Asxl1 and binds both WT and mutant Asxl1. FLAG antibody interacts exclusively with Asxl1 mutant. (B) Bar chart showing genomic distribution of Asxl1 and FLAG (Asxl1 mutant) binding peaks relative to RefSeq functional categories, including promoters (within 5 kb upstream of TSSs), 5′ untranslated regions (UTRs), exons, introns, 3′ UTRs, downstream (within 5 kb downstream of the gene), and intergenic regions (outside −5 to 5 kb of genes). (C) Peak result of H3K4me3, Asxl1, and FLAG (Asxl1 mutant) across Id3 gene in ChIP-seq analysis. (D) Scatterplot of scores of Asxl1 peaks and H3K4me3 (top), H2AK119Ub (middle), and H3K27me3 (bottom) peaks in WT c-Kit⁺ cells. Reads per kilobase of exon per million mapped reads (RPKMs) were color coded as indicated in the bottom. The significance was determined by R² (the square of the Pearson correlation coefficient). (E) Scatterplot of scores of Asxl1 peaks and the ratio of H3K4me3 peaks to H3K27me3 peaks in c-Kit⁺ control cells. RPKMs were color coded as indicated in the bottom. (F) Scatterplot of scores of FLAG peaks and the ratio of H3K4me3 peaks in c-Kit⁺ KI cells to those in c-Kit⁺ control cells. RPKMs were color coded as indicated (top). (G) Motif enrichment analysis of regions where H3K4me3 was reduced in KI c-Kit+ cells. Top motifs are listed.