Figure 4. Butyrate exposure induces complex histone acetylation dynamics that only partially correlate with transcriptional outcomes. RNA-Seq and ChIP-Seq datasets, obtained from butyrate-treated primary human mast cells, were integrated to investigate the relationship between butyrate-mediated controls of histone acetylation and gene expression. (A ) Representative examples of hypo-acetylated (indicated by a blue rectangle) canonical mast cell genes (i.e. BTK , SYK , MRGPRX2 andKIT ). Yellow shading highlight significant differences between histone acetylation in untreated human mast cells (indicated in blue, 0 h) and butyrate treated human mast cells (indicated in red, 24 h). (B ) Histograms of H3K27Ac at the TSS of downregulated genes (left box), unchanged genes (middle box) and upregulated genes (right box). The 0 h timepoint is indicated in light grey and TSS acetylation after butyrate treatment indicated in shades of red. (C ) Quantification of the reduction of TSS acetylation area under the curve at 3, 12 and 24 h after butyrate treatment (with downregulated genes indicated in blue, unchanged genes in yellow and upregulated genes in orange). (D ) Examples of hyper-acetylated genes (i.e.F2RL1 and CLGN ). (E ) Histograms of H3K27Ac at the TSS of the top 50 upregulated genes (left box), top 100 upregulated genes (middle box) and lower 451 upregulated genes (right box). (F ) Area under the curve quantification of data shown in E. (G ) Histograms of H3K27Ac at the enhancer landscape (EL) of downregulated genes (left box), unchanged genes (middle box) and upregulated genes (right box). (H) Area under the curve quantification of data shown in G.