Fig. 2: SOX2 is critical for genome-wide histone acetylation and formation of super-enhancers.

a Heatmap comparison of SOX2 ChIP-seq signals in the control and SOX2 knockdown K450 cells, ranked by SOX2 intensities in control K450 cells. b Genomic distribution of SOX2 ChIP-seq peaks in control K450 cells. Promoter (TSS ± 1000 bp). Statistics of ChIP-seq peaks showing significant enrichment of SOX family transcription factor binding motifs in SOX2 ChIP-seq peaks. c Heatmap analyses of H4ac, H3K27ac and H3K4me3 levels on SOX2 binding regions, ranked by SOX2 ChIP-seq intensities in control K450 cells. d Profiles of SOX2, H4ac, H3K27ac and H3K4me3 ChIP-seq signals from control and SOX2 knockdown K450 cells. e Heatmap comparison of SOX2 binding intensities over ChIP-seq peaks showed reduced levels of H4ac, H3K27ac and H3K4me3 (1.5-fold change) upon SOX2 knockdown, ranked by SOX2 ChIP-seq signals from control K450 cells. All ChIP-seq signals are displayed from −3 kb to +3 kb surrounding the peak center. f Venn diagram analyses of super-enhancers identified in control and SOX2 knockdown K450 cells. g Normalized H3K27ac, H4ac and SOX2 ChIP-seq signals of control and SOX2 knockdown K450 cells over the lost, shared and gained super-enhancers upon SOX2 depletion. In a–g one ChIP-seq replicate was performed, and data are shown from two analytical replicates.