Figure 4. Dnmt3a binds a subset of enhancers in tumor cells.
(A) Schematic representation of a short treatment of DMBA/TPA in wild-type and Dnmt3a-cKO animals. (B) Genomic localizations of Dnmt3a determined by ChIP-seq of Dnmt3a in epidermal cells isolated from wild-type animals after 6 weeks of DMBA/TPA treatment. (C) Gene ontology analysis of the 363 H3K27ac-enriched regions (located at least 4 kb away from the TSS) also bound by Dnmt3a in isolated epidermis from wild-type animals after 6 weeks of DMBA/TPA. (D) Screenshot of enhancers bound by Dnmt3a in DMBA/TPA-treated skin in the FOS locus. All tracks are normalized to the number of mapped reads.
Figure 4—figure supplement 1. Deletion of Dnmt3a alters the expression of genes involved in proliferation, lipid metabolism, epidermal differentiation, and Wnt signaling, after 6 weeks of DMBA/TPA treatment.
(A) Left panel, heatmaps representing gene expression (rlog transformed values) of the 498 genes in sorted bulge hair follicle stem cells (Bulge) (Itga6bright/CD34pos) that were differentially expressed between wild-type (n = 3) and Dnmt3a-cKO (n = 3). Right panel, gene ontology analysis of the 498 differentially expressed genes up- or downregulated in Dnmt3a-cKO mice as compared to their wild-type littermates. (B) Left panel, heatmaps representing gene expression (rlog transformed values) of the 188 differential expressed genes between wild type (n = 4) and Dnmt3a-cKO (n = 4) sorted interfollicular epidermal (IFE) basal cells (Itga6bright/CD34neg). Right panel, gene ontology analysis of the 188 differentially expressed genes that were up- or downregulated in Dnmt3a-cKO mice as compared to their wild-type littermates.