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Fig. 4 | Epigenetics & Chromatin

Fig. 4

From: MEK inhibition remodels the active chromatin landscape and induces SOX10 genomic recruitment in BRAF(V600E) mutant melanoma cells

Fig. 4

MEK inhibition induces extensive SOX10 chromatin binding in 501mel cells. a Venn diagram showing overlap of SOX10 ChIP-Seq peaks in DMSO- and AZD6244-treated 501mel cells. In both treatment groups, the number of SOX10 ChIP-Seq peaks represents the total that were replicated across two independent experiments. Significance cutoff for SOX10 ChIP-Seq peaks was p < 1e10−5. b Genomic distribution of differentially bound SOX10 peaks in 501mel cells (AZD6244 vs DMSO) with respect to the nearest TSS as revealed by GREAT (using the basal plus extension settings). Values on the Y-axis represent percent of peaks found in a given genomic bin relative to TSS, i.e., [0, 5 kb], [5 kb, 50 kb], [50 kb, 500 kb], [500 kb, infinity]. c Heatmap of SOX10 ChIP-Seq signals at genomic regions that lost H3K27ac (upper panel) or gained H3K27ac (lower panel) in response to AZD6244 treatment (in units of read per million of genomic region). Each row shows a ± 5 kb region centered on an H3K27ac region, and rows are ordered by SOX10 ChIP-Seq signal. d Line plots showing average SOX10 ChIP-Seq signal intensities (y-axis) across regions losing H3K27ac (upper panel) and gaining H3K27ac (lower panel) over a ± 5 kb genomic window centered on differentially remodeled H3K27ac sites (x-axis)

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