Supplementary Figure 3: STAT4 and STAT1 differentially promote remodeling of chromatin in activated NK cells.
From: Epigenetic control of innate and adaptive immune memory
(A) Frequency polygon of log2 fold changes from differentially accessible (DA) regions (FDR < 0.05) comparing STAT-deficient NK cells to WT cells two days post infection. Counts have a bin width of 0.2. (B) Heatmap of log2 fold changes of gene expression comparing with Stat4–/– or Stat1–/– to WT two days post infection. Shown are genes that are commonly differentially expressed (FDR < 0.05) in both conditions. (C) Bar plots of RNA-seq normalized counts of all STAT family genes in both uninfected and infected NK cells in Stat4–/–:WT (blue) or Stat1–/–:WT (green) two days post infection. Data represent mean ± s.d; *padj < 0.05 as calculated by DESeq2. (D) Pairwise overlap of ChIP-seq, RNA-seq, and ATAC-seq results. P-values were calculated by hypergeometric tests using all annotated genes for “common genes” tests and a union of accessible and occupied peaks for “common peaks” tests. (E) Differential expression (FDR < 0.05) of overlapping genes indicated in Fig. 3e from Stat1–/–:WT NK cells two days post infection. (F) Genomic tracks of aligned STAT1-ChIP-seq and Stat1–/–:WT ATAC-seq data. y-axis depicts normalized counts, while x-axis displays genomic axis with scale bar. Bar plots quantify number of reads within highlighted peak regions (dashed lines) shown as mean ± s.d.
