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. 2022 Jul 15;119(29):e2202015119. doi: 10.1073/pnas.2202015119

Fig. 1.

Fig. 1.

Epigenetic states of H3K27ac and the effect of Sox9 manipulation in 3xCr HGG and ZRFUS EPN tumor subtypes. (A) Schematic of IUE to generate HGG and EPN in a native mouse model. (B) Comparison showing heatmaps of ChIP-H3K27ac signal at 4 kb from peak center at transcription start site (TSS) in 3xCr HGG and ZRFUS EPN tumors. (C) Pie charts showing the percentage of total H3K27ac sites that carries the Sox9 motif allowing 0 mismatch at 1,000 bp from peak center. (D) Comparison of active H3K27ac peaks between mouse 3xCr HGG and 10 human HGG patient tumors. (E) Comparison of active H3K27ac peaks between mouse ZRFUS EPN and 10 human Rela-fusion-positive EPN patient tumors. (F) Kaplan–Meier survival curves of 3xCr HGG control (n = 23), Sox9-LOF (n = 31), and Sox9-GOF (n = 39). (G and H) Representative images of BrdU staining on P90 3xCr HGG tumors and box plots showing quantification of BrdU over DAPI-labeled cells (n = 3 mice per group, 2 sections each; scale bar: 50 μm). (I) Kaplan–Meier survival curves of ZRFUS EPN control (n = 41), Sox9-LOF (n = 20), and Sox9-GOF (n = 25). (J and K) Representative images of BrdU staining on P70 ZRFUS EPN tumors and box plots of quantification of BrdU over DAPI-labeled cells (n = 3 mice per group, 3 sections each; scale bar: 50 μm). P values in Kaplan–Meier curves were calculated using the log-rank test. P values in box plots were calculated using one-way ANOVA with Tukey’s test (*P < 0.05, ***P < 0.001).