Fig. 5 | Nature Communications

Fig. 5

From: H3K27M induces defective chromatin spread of PRC2-mediated repressive H3K27me2/me3 and is essential for glioma tumorigenesis

Fig. 5The alt text for this image may have been generated using AI.

H3K27M confers tumorigenicity in vivo. a Survival of mouse orthotopic xenograft cohorts injected with BT245 (K27M; n = 18 mice, K27M-KO; n = 19 mice, log-rank test) and DIPGXIII lines (K27M; n = 3 mice, K27M-KO; n = 3 mice, log-rank test). b A model of H3K27M reversibly inhibiting the spread of H3K27me2 and H3K27me3 deposition by PRC2 from initial recruitment sites. Note that while in H3K27M H3K27me3 mark is restricted to unmethylated CGIs, H3K27me2 is found in domains where there is H3K27me3 in non-K27M condition. Source data are provided as a Source Data file

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