Fig. 3: Chromatin regulators are disrupted by alternative splicing in pHGG.

a Gene set enrichment analysis of chromatin-modifying enzymes among genes differentially spliced (left) or differentially expressed (right) in pHGG. NES normalized enrichment score, FDR false discovery rate. b Protein–protein interactions between chromatin-related proteins that are differentially spliced in pHGG were retrieved from STRING. Edge thickness represents interaction confidence. SWI/SNF mammalian switch/sucrose-nonfermentable, NuRD nucleosome remodeling and deacetylase, PRC1.1 polycomb-repressive complex 1.1, CERF CECR2-containing remodeling factor complex. c Heatmap of percent inclusion (ψ) of differential splicing events (|Δψ| >0.15, FDR < 0.05) identified between pHGG (n = 64) and normal brain (n = 20) in SWI/SNF complex members. d Gene set enrichment analysis (GSEA) of SWI/SNF target gene enrichment among genes differentially spliced in pHGG. NES normalized enrichment score, FDR false discovery rate. e Proportion of SWI/SNF target genes whose ψ correlates significantly (Benjamini–Hochberg corrected P < 0.05) with ψ of each SWI/SNF complex member across pHGG samples (n = 64), or with the maximally variant complex member (“All”) in each sample. f Percentage of chromatin regulators with differential ASE predicted to affect structural domains and intrinsically disordered domains (IDR) mapped in UniProt. g Percentage of chromatin regulators with differential ASE predicted to affect post-translational modification (PTM) sites mapped in UniProt. Statistical tests: t test with Benjamini–Hochberg multiple hypothesis testing correction (e). Source data are provided as a Source Data file.