Fig. 4: TP63 is a mediator of tumour-specific chromatin contact.

A Scatter diagram of SDOC alteration correlated with TFBS in BERP35T1 and BERP35T4. The color and size represent log2 STD of gene expression alteration in BERP35T1 (left) and BERP35T4 (right). B Average chromatin accessibility levels at binding sites of each TF in normal BEP2D cells (x-axis) and tumour cells (y-axis) measured as reads per kilobase of transcript per million reads mapped (RPKM). The pink and green dashed lines correspond to 3-fold increases and 3-fold decreases, respectively, in ATAC-seq read abundances in tumor cells. The names of TFs that were significantly upregulated and showed an increase in the ATAC-seq read abundance of more than 3-fold in either tumour cell line are indicated. FPKM log2 fold change of each differentially expressed TF were marked by different sizes and color. C Bar plots showing the fractions of putative TP63 binding sites in all putative TFBSs located within the 3 groups of gained-in-tumour ATAC-seq peaks (Left bar in each panel: ATAC-seq peaks gained in tumour cells and located at contact-decreased loci; middle bar in each panel: ATAC-seq peaks gained in tumour cells and located at contact-unchanged loci; right bar in each panel: ATAC-seq peaks gained in tumour cells and located at contact-increased loci). Significance: **P < 0.01, ***P < 0.001, two-sided Fisher’s exact test. D Bar plots showing the fractions of ATAC-seq peaks colocalized with P63 ChIP-seq peaks in the 3 groups of loci. Loci were grouped by the number of other distal loci that showed concomitantly increased, unchanged or decreased contact frequencies in tumour cells. ChIP-seq data is from Sato et al. (Cancer Research, 79(24), 6084–6100.). Significance: *P < 0.05, **P < 0.01, ***P < 0.001, two-sided Fisher’s exact test.