NOX2-deleted AMs acquire epigenetic alterations. (A) An MDS plot of AM ATAC-seq peak signals in 2 different dimensions showing differences among the indicated groups of mice (n = 3 independent samples in each group). (B) Histogram comparing aggregate ATAC-seq peak heights around TSSs (±500 kb) in various groups for the genes with significant differences between Cybb^KO CD11b^high AMs and WT CD11b^low AMs from 12-week-old mice. (C) Venn diagram showing the overlay of genes with significant alterations in both RNA-seq and ATAC-seq (TSS, ±500 kb) among various groups. (D) Representative WUSTL epigenome browser tracks displaying normalized ATAC-seq peak signal distribution in selected genes from AMs sampled from the indicated groups of 4- and 12-week-old WT and Cybb^KO mice along with CHIP-seq data for H3K4Me1 and H3K27ac marks from Lavin et al.⁵⁸ Boxes indicate ATAC-seq peaks that are significantly different in 12-week-old Cybb^KO samples compared with 12-week-old WT samples. (E) Hallmark gene set analysis for genes with altered ATAC-seq peak signals between Cybb^KO CD11b^high and WT CD11b^low as well as Cybb^KO CD11b^high and Cybb^KOCD11b^lowAMs. (F) HOMER de novo motif enrichment analysis for transcription factor binding sites in open chromatin ±500 kb from the TSS, as identified in ATAC-seq, as analyzed in AMs sampled from 12-week-old mice (n = 3 independent samples in each group). The percentage of motif occurrence in peaks vs background is also shown. CHIP, chromatin immunoprecipitation; HOMER, hypergeometric optimization of motif enrichment; MDS, multidimensional scaling; TSS, transcription start site.