Fig. 3: Loss of KDM5C, KDM6A or KMT2B induced a genome-wide changes in chromatin accessibility that correlates with transcriptomic dysregulation. | Communications Biology

Fig. 3: Loss of KDM5C, KDM6A or KMT2B induced a genome-wide changes in chromatin accessibility that correlates with transcriptomic dysregulation.

From: Multi-omics elucidation of KDM5C, KDM6A, and KMT2B roles in cancer epigenetic dysregulation and transcriptional reprogramming

Fig. 3

MA plot of ATAC-seq peaks comparing KDM5CKO to WT cells (a), KDM6AKO to WT cells (b), and KMT2BKO to WT cells (c). The numbers of peaks with significant changes (|log2FC| > 0.263, FDR < 0.05, redpoints) were shown. d Pie charts showed the percentage of differentially accessible ATAC-seq peaks (|log2FC| > 0.263, FDR < 0.05) at promoter, intronic, intergenic and exonic regions. e Heat map of differentially accessible ATAC-seq peaks described in a (|log2FC| > 0.263, FDR < 0.05) in a 5-kilobase (kb) window grouped by localization at promoter, intron and intergenic regions. f Distribution of chromatin accessibility changes associated with significantly upregulated (red) or downregulated (blue) genes comparing KDM5CKO, KDM6AKO, KMT2BKO, with WT cells. p values were calculated using a two-sided Kolmogorov–Smirnov (KS) test comparing peaks associated with differentially expressed genes to all genes.

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