Fig. 3: Class I and class II pancreatic enhancers largely map to distinct gene regulatory elements.
a Tag density plots for class I and class II pancreatic enhancers displaying ATAC-seq (top) and H3K4me1 ChIP-seq (bottom) read density in GT and PP2. Plots are centered on FOXA1/2 peaks and span 5 kb. b Box plots of ATAC-seq (top) and H3K4me1 ChIP-seq (bottom) counts at class I and class II pancreatic enhancers in GT and PP2 for control and FOXA1/2−/− cells (P = < 2.2 × 10−16, <2.2 × 10−16, 0.01, and <2.2 × 10−16 for control versus FOXA1/2−/− of ATAC-seq signal at class I in GT, class I in PP2, class II in GT, and class II in PP2, respectively. P = < 2.2 × 10−16, 0.01, 0.02, and 0.01 for control versus FOXA1/2−/− of H3K4me1 signal at class I in GT, class I in PP2, class II in GT, and class II in PP2, respectively; Wilcoxon rank sum test, 2-sided). Plots are centered on median, with box encompassing 25th–75th percentile and whiskers extending up to 1.5 interquartile range. c Percentage of FOXA1- and/or FOXA2-bound pancreatic super-enhancers (SEs) in PP2 containing only class I, only class II, or both class I and class II enhancers. d Percentage of chromatin loop anchors in PP2 containing only class I, only class II, or both class I and class II enhancers. e Percentage of genes associated with only class I, only class II, or both class I and class II enhancers. Target genes were assigned to enhancers based on nearest TSS of expressed genes (fragments per kilobase per million fragments mapped (FPKM) ≥ 1) in PP2. f Schematic illustrating FOXA1/2 occupancy, chromatin accessibility, and presence of H3K4me1 and H3K27ac at class I and class II enhancers in GT and PP2. All ChIP-seq and ATAC-seq experiments, n = 2 replicates from independent differentiations.
