Fig. 6. Promoter enrichment of histone succinylation and relationship with transcription.

a Merged numbers of H3K23su, Ksu, and H3K27ac peaks detected in TSA-treated and TSA-untreated HeLa cells by ChIP-seq. ChIP-seq experiments were carried out with three independent biological samples. b Sorted and centered heatmaps showing peak intensities of H3K23su, Ksu, and H3K27ac in TSA-treated and TSA-untreated HeLa cells. c The average plot showing that TSA treatment led to markedly increased intensities of H3K23su, Ksu, and H3K27ac peaks. d Genomic feature distribution of H3K23su peaks. The relative proportions of H3K23su peaks in the TSS, 5’UTR, exons, introns, 3’UTR, and intergenic regions in TSA-treated and TSA-untreated HeLa cells are displayed. e Venn diagram showing the number of H3K23su peaks that show co-occupancy with H3K4me3 peaks and H3K27ac peaks in TSA-treated and TSA-untreated cells. f Meta gene analysis showing H3K23su occupancy profiles in TSA-treated and TSA-untreated cells. Note that TSA treatment drastically elevated H3K23su TSS occupancy. g IGV browser snapshots showing the distribution of reads around the TSS of the actively transcribed CCND1 gene for the indicated histone modifications and RNA-seq. h Number of genes that were upregulated or downregulated by TSA treatment detected by RNA-seq analysis. i Box plots comparing the expression levels of genes with and without H3K23su peaks in their TSS regions in control (DMSO) treated cells. Integrated ChIP-seq and RNA-seq data analyses were carried out with three independent biological replicates. j Box plots showing the relationships between H3K23su peak intensity at TSSs and levels of transcription. Three groups of genes were categorized according to the levels of H3K23su peak intensity at TSSs.