Fig. 7

K27M-Driven Chromatin Remodeling and Transcriptional Regulation of CDKN2A and HGF. (A) Bar plot showing CDKN2A expression (RNA-seq) and chromatin accessibility (ATAC-seq log2FC) in K27M and PRC2 mutant cells relative to their wild-type counterparts. Increased chromatin accessibility in K27M mutants suggests that K27M-specific transcriptional regulation of CDKN2A is partially mediated through chromatin remodeling. EZH1/2 knockout alone does not alter chromatin accessibility or expression of CDKN2A, indicating that PRC2 loss alone is not sufficient for CDKN2A activation. (B) Bar plot illustrating HGF expression (RNA-seq) and chromatin accessibility (ATAC-seq log2FC) in K27M and PRC2 mutant cells. While HGF is significantly upregulated in K27M mutants, ATAC-seq analysis does not indicate corresponding chromatin accessibility changes. This suggests that HGF regulation is independent of chromatin opening and may instead be controlled by transcriptional or enhancer-based mechanisms