Fig. 6
EOMES induces epigenetic changes in enhancer regions. a MA plot of mean ATAC-seq counts per peaks showing the differentially open regions (DOR) of CD8SP WT (blue) and EomesTg (red) cells with the indicated number of regions. Histograms indicate the number of opening or closing regions in EomesTg in comparison to WT cells at promoters and enhancers. b Cumulative distribution plot generated by BETA algorithm showing the predicted activating/repressive functions of DOR in CD8SP WT and EomesTg with the indicated P-values determined by the Kolmogorov–Smirnov test. c Scatter plots display differentially active H3K27ac peaks at promoters (left) and enhancers (right) in CD8SP WT (blue) and EomesTg (red) cells. d CiiiDER analysis for putative transcription factors motifs from DOR of CD8SP EomesTg and WT at enhancers. Transcription factors are coloured according to their gene coverage P-value and whether they are over- (red) or under- (blue) represented. The size of each point is also proportional to log10 P-value. e Normalized coverage plot of histone modifications (H3K4me1, H3K4me3 and H3K27ac) and chromatin accessibility (ATAC-seq) centred on EOMES-binding sites at promoters and enhancers annotated to genes from Fig. 5e. f Representative ChIP-seq tracks of H3K4me1, H3K27ac, ATAC-seq, EOMES, and RUNX3 from the indicated population at the enhancers of Cxcr3 and Il2rb loci highlighted in grey. ChIP-seq was performed on three independent IPs (n = 3 mice per sample). ATAC-seq was performed on two independent samples (n = 2 mice per sample) from each group
