Genome-wide analysis of chromatin accessibility in WT and Bach2-deficient Treg cells. (A) Representative alignments of ChIP-Seq measurements showing binding of BACH2 and p300 at the indicated loci and RNA-Seq measurements from EGFP⁺ Treg cells from tamoxifen-treated Bach2^+/+Foxp3^{EGFP-Cre-ERT2} (WT) and Bach2^fl/flFoxp3^{EGFP-Cre-ERT2} (CKO) animals. Representative alignments of RNA-Seq from three biological replicates per genotype are shown. (B) Differential analysis of global chromatin accessibility within Foxp3^{EGFP-Cre-ERT2+} Treg cells from tamoxifen-treated Bach2^+/+Foxp3^{EGFP-Cre-ERT2} (WT) and Bach2^fl/flFoxp3^{EGFP-Cre-ERT2} (CKO) animals. Mean ATAC-Seq signal at called ATAC-Seq peaks (peak calling threshold FDR < 0.05; binomial distribution) are shown as points. Significantly differentially accessible peaks between genotypes (FDR < 0.1; Wald test with Benjamini–Hochberg correction) are indicated as red points (227 peaks UP in WT and 214 peaks DOWN in WT; FDR < 0.1). (C) Histogram showing mean ATAC-Seq signal around called ATAC-Seq peak centers which either overlap (left) or do not overlap (right) BACH2 binding sites (peak calling threshold FDR < 0.05; binomial distribution). Data are representative of three ATAC-Seq and RNA-Seq replicates per genotype.