Runx1 shapes the chromatin landscape via a cascade of direct and indirect targets
Fig 3
Runx1 Deletion Alters Chromatin Accessibility Despite the Presence of Runx2.
A) Venn diagram of ATAC-seq peaks in control and Runx1KO cells showing the number of regions open in both cell lines (Runx1-independent), regions open only in control cells (Runx1-dependent) and regions open only in Runx1KO cells (Runx1KO-induced). B) Heatmaps of the ATAC-seq reads mapping to Runx1-independent, Runx1-dependent, and Runx1KO-induced peaks in the control and Runx1KO cells. C) Graph of the -log10 p-values of motif enrichment, displaying that Runx1-dependent ATAC-seq peaks are strongly enriched for AP-1 and Runx motifs. D) Gene set enrichment analysis showing enrichment of transcriptionally down-regulated genes (in blue and up-regulated in red) by Runx1-dependent ATAC-seq peaks that are bound by Runx1. E) Heatmap showing Runx1-Dependent ATAC-seq regions bound in Runx1 and Runx2 ChIP experiments. F) Genomic snapshots of Gdnf and Pak3 genes that are downregulated in Runx1KO cells showing open chromatin regions present in control cells but not Runx1KO cells that are bound by Runx1 and Runx2 and retain Runx2 binding in the Runx1KO cells. G) Genomic snapshot of the Runx1KO downregulated gene Osr1 that has genomic regions that lose chromatin accessibility in Runx1KO cells, which are bound by Runx1 and Runx2 in control cells, with reduced Runx2 binding in Runx1KO cells.