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.