Analysis of the TAp63 binding landscape. (A) Overlap between TAp63 binding sites in primary cells from 1 CLL case as well as MEC1 cell line as identified using a stringent MACS peak calling cutoff q = 0.00001. One hundred and twenty common genes were found between the 2 comparison groups. (B) Genomic distribution of TAp63 binding sites in both samples. Promoter binding corresponds to 17% and 11.4% in CLL and MEC1 cells, respectively. (C) De novo motif analysis for the TAp63 binding sites in both samples identified a motif resembling the p63 (matrix id in the JASPAR motif database: MA0525.2)-p53 (matrix id: MA0106.3)-p73 (matrix id: MA0861.1) family of motifs as the most statistically significant (e-value: CLL cells, 2.5e-146; MEC1, 8.7e-476). (D) IGV genomic browser snapshots depicting the TAp63 binding profile and epigenomics marks on the MDM2 locus. A promoter-proximal strong TAp63 binding was found at the MDM2 gene, confirming its characterization as a well-described positive TAp63 transcriptional target. (E) IGV genomic browser snapshots illustrating the TAp63 binding events and epigenomics marks at the BCL2 locus in a region previously characterized as a super-enhancer in CLL. (F-G) Co-depiction of TAp63 binding signals with publicly available ATAC-seq (GEO no. GSM3382058) and H3K27ac (GEO no. GSM3382050) data around its total binding sites in both samples using an aggregate plot (top half of the scheme) and a heatmap (bottom half of the scheme) analysis TAp63 binding sites coexist with ATAC-seq and H3K27ac signals, corresponding to accessible and active chromatin. MACS, model-based analysis of ChIP-seq.