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. 2019 Jan 15;47(5):2349–2364. doi: 10.1093/nar/gky1317

Figure 5.

Figure 5.

KDM3A regulates H3K27ac and TEAD1 binding on enhancers. (A, B) ChIP analysis shows TEAD1 enrichment in KDM3A WT and KO cells lines. KDM3A depletion attenuates TEAD1 recruitment to CTGF under all three conditions (A), while on CYR61 only during FBS treatment (B). (C) ChIP analysis shows H3K4me1 and H3K27ac enrichment on CYR61 enhancers in KDM3A WT and KO cells lines. The locations of two enhancers are shown at the bottom. (D) The average H3K9me2, H3K27ac and TEAD1 enrichment on all TEAD1 target sites. (E) Heat map shows the expression (FPKM) and clustering of TEAD1 target genes. (F) The average H3K9me2, H3K27ac and TEAD1 enrichment on enhancers of KDM3A-dependent genes. (G) ChIP assays to show p300 enrichment on CYR61 enhancer under starvation and FBS treatment. (H) Co-immunoprecipitation of p300 and KDM3A in HCT116 cells under starvation and FBS treatment. • labelled non-specific bands. * means P-value ≤ 0.05, ** for P-value ≤ 0.01. The results in all histograms represent the means (±SD) of at least three independent experiments. The sequencing data were obtained from two biological replicates.