Supplementary Fig. 7: Loss of MTHFD1 binding after BRD4 degradation.

a, Representative genome browser view of BRD4 and MTHFD1 binding in the H3K27ac-marked promoters of KEAP1 (left) and TFAP4 (right). All ChIP tracks were normalized to total mapped reads and the respective IgG control was subtracted from the merged replicate tracks. b, Enrichment of BRD4 and MTHFD1 ChIP signal in H3K27ac peaks. Peaks were sorted by total signal abundance and data represent merged replicates normalized to 1X genome coverage. c, Volcano and scatterplots comparing binding in dBET6- or DMSO-treated cells, with significantly bound sites (FDR adjusted p-value < 0.1 and absolute log2 fold change > 1) marked in red. Differential regions were discovered with the Wald test using the DiffBind package with n = 2 biologically independent experiments. P-values were adjusted with the Benjamini-Hochberg method. d, Normalized ChIP-seq signal in differential regions bound by MTHFD1 or BRD4 upon dBET6 treatment. e, Quantification of global differences in differentially bound MTHFD1 or BRD4 sites upon dBET6 treatment. A two-sided Mann-Whitney U-test was used to assess significance. f, Number of ChIP-seq peaks detected for each protein in WT cells. g, Amount of overlap between peaks of MTHFD1, BRD4 or H3K27ac in dBET6- or DMSO-treated cells measured by the fractional overlap, total intersection or the Jaccard index (intersection over the union of peaks).