Fig. 2: Epigenomic characteristics of inducible RelA- and Rel-binding regions in activated B cells.

a–d, Chromatin accessibility and histone modifications were assessed by ATAC-seq and ChIP–seq, respectively, in splenic B cells activated with anti-IgM for 0, 1, 4 and 18 h. a,b, Pre-existing chromatin state in unactivated B cells at sites of inducible RelA binding at 1 h (left) and Rel binding at 18 h (right). Heatmaps were centered on summits of RelA or Rel peaks, ordered based on the strength of ATAC signal and segregated by genomic locations as indicated to the left of each panel. Boxed plots above each heatmap show the average profile across all sites at each genomic ___location (blue = promoters (defined as −1 kb to +0.1 kb relative to the transcription start site), yellow = intergenic regions and green = introns). c, Chromatin accessibility changes induced by activation were determined using DiffBind analysis of ATAC-seq data (fold change ≥ 1.5, FDR ≤ 0.05). Transiently induced ATAC peaks (at 1 h) are shown on the top half (3,143 total peaks) and those induced at 18 h are shown at the bottom (2,261 total peaks), ordered according to the strength of the ATAC signal. H3K4me3 and RelA or Rel ChIP–seq profiles of the corresponding sites at the indicated time points are shown in adjacent panels. Boxed plots above each heatmap show the average ChIP–seq or ATAC-seq profile for each category of inducible ATC peaks (blue = 1 h induced ATAC peaks and green = 18 h induced ATAC peaks). Induced ATAC peaks at 1 h and 18 h were annotated to genomic regions shown on the right. d, Representative browser tracks of ATAC-seq peaks induced at 1 h (Irf4) or 18 h (Dolk/Nup188) and associated RelA or Rel binding at the indicated times. Transcriptional direction and transcription initiation sites are shown by red arrows. mm9 annotations are shown above the tracks.