Fig. 5
H3K18cr and H3K18ac ChIP-seq on MS275-treated HCT116 cells. a Probe trendplot over TSS (±10 kbp) of reads from H3K18ac and H3K18cr ChIP-seq on HCT116 cells with and without MS275 treatment; b H3K18cr and H3K18ac ChIP-seq analysis shows a relative decrease in these marks over TSS upon MS275 treatment, error bars are SEM, n = 3, p < 0.05, paired t-test; c aligned probe plots over TSS (±5 kbp) of reads from H3K18ac and H3K18cr ChIP-seq with and without MS275 treatment, aligned probes were ranked according to read counts in the H3K18cr/MS275 ChIP-seq. d Scatterplot of read counts of H3K18ac versus H3K18cr MACS peaks of control (vehicle treated) cells and e of H3K18ac versus H3K18cr MACS peaks of MS275-treated cells. f Read counts in H3K18cr MACS peaks from control cells versus MS275-treated cells. MACS peaks close (+2 kbp) and within upregulated genes are in red. g Read counts in H3K18ac MACS peaks from control cells versus H3K18ac, MACS peaks of MS275-treated cells, MACS peaks close (+2 kbp) and within upregulated genes are in red. MACS peaks that show an increase in H3K18cr (f) or H3K18ac (g) on MS275 treatment are in blue. For both H3K18cr and H3K18ac, there is a disproportionate larger number of MACS peaks linked to MS275-upregulated genes that also show an increase in H3K18cr (f) or H3K18ac (g) on MS275 treatment compared to those that show a decrease in these modifications (p < 0.0001, χ2 test)
