Figure 6.
BACH1 facilitates G9a and YAP occupancy and decreases chromatin accessibility at VSMC marker genes’ promoters. (A) Heatmaps showed the genome-wide CUT&Tag binding profiles of BACH1 and YAP, ATAC-seq of opening chromatin and at TSS (TSS ± 5 kb). (B) Venn diagram of genes enriched by BACH1, genes enriched by YAP, and genes with opening of the chromatin. (C) Heatmaps of H3K9me2 and opening chromatin at BACH1 enriched regions in Con- and BACH1-overexpressing (BACH1-OE) HASMCs (peak center ± 4kb for H3K9me2 and peak center ± 3kb for ATAC-seq). (D) Signal profiles of ATAC-seq signal at BACH1 enriched regions in Con and BACH1-OE HASMCs. (E) Signal profiles of H3K9me2 with ChIP-seq signal at BACH1 enriched regions in Con and BACH1-OE HASMCs. (F) The mRNA expression of CENPF, FOXK1, LMNA, and BACH1 in HASMCs. RT-PCR showed that CENPF, FOXK1, and LMNA mRNA levels were increased in BACH1 silencing HASMCs compared with the control HASMCs (n = 4 independent experiments, data are mean ± SD. unpaired two-tail t-test). (G) Co-immunoprecipitation of BACH1, YAP and G9a in HASMCs. BACH1 was immunoprecipitated from HASMCs; the amount of YAP and G9a present in the precipitate was evaluated via Western blot.