Fig. 6

JUN and TCF21 regulate chromatin accessibility at CAD loci. a Venn diagram showing the number of overlaps between TCF21-regulated (intersection of TCF21 knockdown upregulated and overexpression downregulated ATAC peaks, q < 0.01) and JUN-regulated (intersection of two JUN knockdown downregulated ATAC peaks, q < 1e−10 and fold change < 0.5) open chromatin regions in HCASMC. b Venn diagram showing the number of overlaps between JUN plus TCF21-regulated open chromatin regions (from a) and TCF21 or JUN peaks (q < 0.01) in HCASMC. g Heatmap distribution of ATACseq for control (Ctrl) or two JUN knockdowns (KD1 and KD2), ATACseq of control (Ctrl) or TCF21 knockdown (TCF21-KD) or TCF21 overexpression (TCF21-OE), and ChIPseq of JUN and TCF21, all centered on JUN plus TCF21-regulated open chromatin regions within a 4-kb window in HCASMC. HNF1A serves as a control transcription factor. d Heatmap distribution of ATACseq peaks for Ctrl, JUN-KD1, or JUN-KD2, and ATACseq of Ctrl, TCF21-KD, or TCF21-OE on genes within 10 kb upstream and 5 kb downstream of the transcription start site, in loci located in JUN plus TCF21-regulated open chromatin regions. e Pattern of ATACseq mapping of open chromatin at the human SMAD3 and CDKN2BAS loci, with JUN knockdown (JUN-KD1, -KD2), TCF21 knockdown (TCF21-KD), or TCF21 overexpression (TCF21-OE). ENCODE-layered H3K27ac data are also shown. f Biological processes and g GAD disease enrichment from DAVID Gene Ontology analysis of genes located in JUN plus TCF21-regulated open chromatin regions. Genes were assigned by GREAT with “single nearest” mode