Fig. 3: YAP-driven epigenetic reprogramming of oral epithelial progenitor cells.

a Left: Heatmaps of YAP CUT&Tag signal in primary cell cultures from N and EY epithelia. YAP binding sites were characterized as gained, lost, and unchanged in EY compared to N. Sites are ordered from the strongest to weakest YAP binding, shown in ±2 kb windows centered at YAP binding sites. Right: Averaged YAP CUT&Tag signal centered at gained, lost, and unchanged YAP binding sites (N = 2, EY = 4 biological replicates). b ATACseq signals at gained, lost, and unchanged YAP CUT&Tag binding sites. Averaged signals of at four biological replicates are shown for N and EY. c H3K27ac CUT&Tag signal centered at gained, lost, and unchanged YAP binding sites. Averaged signals of at least two biological replicates are shown. d Binding and expression target analysis (BETA): red, blue and black lines represent cumulative percent of genes that are activated, repressed, or unaffected by YAP. P values were calculated by two-sided Kolmogorov–Smirnov tests (YAP and H3K27ac CUT&Tag: N = 2, EY = 4 biological replicates; RNAseq: N = 4, EY = 6 biological replicates). e MSigDB Hallmark Pathways enriched in the top 200 YAP-activated genes based on BETA were identified using Enrichr^91,92. f Top Venn: Overlap of genes near EY-gained chromatin accessibility by ATACseq and EY-gained H3K27ac CUT&Tag peaks. Bottom Venn: Genes with EY-gained chromatin accessibility and H3K27ac peaks overlapped with EY-upregulated genes by RNAseq and genes near EY-gained YAP CUT&Tag peaks. g Gene Ontology biological processes enriched in the 346 EY-upregulated genes with EY-gained YAP CUT&Tag, H3K27ac, and ATACseq peaks using Enrichr. H3K27ac CUT&Tag: N = 2, EY = 4 biological replicates; ATACseq: 4 biological replicates per condition; RNAseq: N = 4, EY = 6 biological replicates^91,92.