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. Author manuscript; available in PMC: 2019 Dec 1.
Published in final edited form as: Cancer Discov. 2018 Oct 1;8(12):1632–1653. doi: 10.1158/2159-8290.CD-18-0657

Figure 5. TET2 deficiency results in reduction of enhancer cytosine hydroxymethylation and histone acetylation.

Figure 5.

A, Genomic distribution of 5hmC peaks in GC B-cells from Vav-Cre/Tet2+/+ and Vav-Cre/Tet2−/− mice. B, Overlap of 5hmC peaks with enhancers in Vav-Cre/Tet2+/+ GC B-cells. C, D, Number (C) and genomic distribution (D) of DHMR between Vav-Cre/Tet2+/+ and Vav-Cre/Tet2−/− GC B-cells. E, Heatmap of the 5hmC enrichment in all DHMR overlapping with distal enhancers in Vav-Cre/Tet2+/+ and Vav-Cre/Tet2−/− GC B-cells. Region spans 1 kbp up and down from the DHMR’ peak center. Heatmap was generated using deeptools (73). F, Minus log 10 of the FDR scores for the enrichment of 11 gene sets involved in the exit of GC B-cells from the GC. FDR scores were obtained using hypergeometric test for a total of 1825 genes with enhancers overlapping with DHMR. G, Correlation of differential hydroxymethylation in distal enhancers and differential gene expression between Vav-Cre/Tet2+/+ and Vav-Cre/Tet2−/− GC B-cells. H, GSEA enrichment plots showing correlation of genes associated with peaks losing 5hmC and H3K27ac signals. I, Normalized gene expression level of 253 leading edge genes associated with peaks losing 5hmC and H3K27ac signals in Vav-Cre/Tet2−/− and VavP-CrebbpKD B cells, respectively. J, Aggregation plots of 5hmC and H3K27ac enrichment in peaks losing both signals, associated with 253 genes shown in figure 5I.