Fig. 4

Mutation of the DBD of FOXM1 inhibits binding genome-wide. a Hierarchical clustering analysis of the WT and DBD mutant GFP-FOXM1 replicate ChIP-seq datasets showing that the samples separate well into distinct treatment groups. b Venn diagram showing the overlap between binding regions identified by ChIP-seq analysis in 293 cells expressing GFP-FOXM1 WT and the GFP-FOXM1 mutants H287A or R286A. c CEAS analysis comparing genomic distribution of GFP-FOXM1 binding events in WT versus DBD mutants. d Examples of genomic regions showing three representative promoter binding sites in which binding peaks are only identified for GFP-FOXM1 WT and are not present in the DBD mutant cell lines. e Motifs enriched in WT GFP-FOXM1 and the mutant R286A-H287A (full list in Additional file 1: Table S4). P values and percentages in brackets represent the statistical significance and the percentage of peaks for each motif, respectively. Motif sequences are sorted according to their proportional representation in WT GFP-FOXM1 peaks (NS = non-significant)