Fig. 2
From: HDAC inhibitors cause site-specific chromatin remodeling at PU.1-bound enhancers in K562 cells
Chromatin accessibility changes are associated with transcriptional changes from HDACi treatment. Overlap between sets of up (a)- or down (b)-regulated genes (FDR < 0.05) following 72-h NaBut (n = 3 replicates) or SAHA treatment (n = 2 replicates) of K562 cells. Association of chromatin accessibility changes with nearby changes in gene expression resulting from NaBut (c) or SAHA (d) treatment. Plots show the cumulative fraction of genes exhibiting that level of fold-change in expression on the x-axis. Sets of all expressed genes, genes closest to an opened DHS site, genes closest to a closed DHS site, genes closest to 2 or more opened DHS sites, and genes closest to 2 or more closed DHS sites are plotted. Mann–Whitney test used to assess significance between gene sets and all expressed genes. e, f Luciferase assay results for eight DHS sites cloned in front of a minimal promoter (pGL4.23) that open following HDACi treatment, and a known strong enhancer (SE) control. Data points show 12–18 replicates per construct with mean and standard deviation in black. Blue points mark level of normalized luciferase activity in K562 cells with vehicle control (1× PBS or DMSO) added and points in red show level of normalized luciferase activity with 1 mM NaBut or 1 μM SAHA added for 24 h. Note y-axis is on log scale. Asterisk (*) denotes significant by Bonferroni-corrected two-sided T test (P = 2.8 × 10−13, 2.4 × 10−15, 3.6 × 10−7, 1.6 × 10−10, 4.5 × 10−12, 0.17, 1.8 × 10−12, and 3.5 × 10−5 from left to right for NaBut; P = 8.1 × 10−8, 5.0 × 10−6, 2.2 × 10−4, 0.0016, 3.0 × 10−7, 0.65, 3.7 × 10−4, and 0.0040 from left to right for SAHA)