Fig. 2: TFAP2A-dependent epigenetic transcriptional profiles in UM.

A Normalized ChIP-seq tracks for H3K27ac, H3K4me1, TFAP2A and EP300, ATAC-seq and RNA-seq at the TFAP2A loci in OMM2.3 cells; ChIP-seq read signals (y axis) were normalized to the RPKM value in the corresponding sample. B TFAP2A peak distribution in the OMM2.3 cell line. The scatter plot is accompanied by a bar plot and upset plot showing the amounts of TFAP2A in intronic, exonic, intergenic or promoter-proximal sites. C Chromatin states in OMM2.3 cells (left) and relative TFAP2A density (right). States were defined using ChIP-seq data for all histone modifications using the hidden Markov modelling algorithm (ChromHMM). Frequency refers to the probability of each mark being present in a given state. D Heatmaps of TFAP2A density in OMM2.3 cells are shown accordingly. Normalized ChIP-seq tracks for H3K27ac, H3K4me1, and TFAP2A transcription factors at TF2P2A binding loci in OMM2.3 cells. ChIP-seq read signals (y-axis) were normalized to the RPKM value in the corresponding sample. E Representative heatmaps of H3K27ac density in the OMM2.3 cell line and UM tissue. Differences between cell lines and tumour tissue at common enhancer sites and significantly enriched enhancer sites are shown.