Fig. 3: PLAGL family motifs are highly enriched in human ZR EPN compared with PF-EPN.

a, Schematic of human snMultiome data generation from 21 patients, including ZR fusion-driven EPN (N = 6), PLAG/L fusion-driven tumours (N = 5) and PF-EPN (N = 10). b, Integrated snMultiome data from 21 patients with initial cell type annotation. UMAP was generated by joint analysis of snRNA and snATAC data using the weighted nearest-neighbour method. c, Tumour cells were categorized into non-malignant and malignant types according to their degree of CNV. d, Analysis of malignant tumour cells using tumour-specific gene expression markers classified patients into three molecular groups (PF-EPN, PLAG/L fusion and ZR EPN). Specific group characteristics were further validated by DNA methylation analysis. e, The ZR fusion signal in malignant cells was assessed across samples by expression of the 93-gene signature. f, Heatmap showing genes with significant differential expression among malignant cells predicted in the three tumour groups. TF-encoding genes with significant expression differences are highlighted. g, Heatmap displaying the top 100 differential snATAC peaks identified for each group. Motif enrichment was predicted separately for each group on the basis of the top 100 peaks, with the top 10 enriched motifs highlighted alongside the associated gene names. PLAG family motifs are highlighted in red. h, PLAG family motif activity in each tumour type. i, Comparison of the proportion of cells exhibiting open chromatin at the ZR binding region between the ZR and PLAG/L groups. Orange dots indicate regions in which the proportion of cells with open ZR binding sites was more than twofold higher in the ZR group compared with the PLAG/L group. Black-highlighted dots represent ZR fusion target genes. The green dotted line represents the regression line.