Fig. 1.

Ezh2 loss worsens DMG pathogenesis while overexpression delays the disease. DMGs was induced by injecting DF1 cells infected with RCAS-PDGF-B, CRE, shp53-RFP and RCAS-Y/RCAS-CRE viruses in P4 pups from Ntv-a;Ezh2^fl/fl mice. a. Schematic representing establishment of EZH2 loss-of-function DMG mouse model. b. Representative H&E staining of tumors from EZH2 WT and EZH2 LOF mice, scale bar = 500 µm. c. Kaplan–Meier survival curve of EZH2 WT and EZH2 LOF mice, p = 0.0847 by Gehan-Breslow-Wilcoxon test,ns, not significant. d. Tumor grades determined in both groups are shown. e. Representative Ki-67 staining from both groups is shown, scale bar = 100 µm (top) and quantitation of staining, (p = 0.02, unpaired t-test n = 5 tumors/group, bottom). f. Representative EZH2 and H3K27me3 staining from both the groups is shown, scale bar = 100 µm and quantitation of EZH2 (p = 0.02, unpaired t-test n = 3 tumors/group) and H3K27me3, (p < 0.001, unpaired t-test n = 5 tumors/group). g. Quantitation of BrdU incorporation by cell proliferation assay after treatment with EPZ011989 (1 µM) in P3 neural precursor cells infected with RCAS-PDGF-B, RCAS-shp53RFP and RCAS-Y/RCAS-CRE viruses, (bottom, p < 0.0001, unpaired t-test, n = 5 independent experiments). h. Representative IHC staining for both groups for Nestin, Olig2 and GFAP (scale bar = 100 µm)