Fig. 2: Significant enrichment of PLAGL family motif activity in ZR fusion tumour cells. | Nature

Fig. 2: Significant enrichment of PLAGL family motif activity in ZR fusion tumour cells.

From: Dominant clones leverage developmental epigenomic states to drive ependymoma

Fig. 2: Significant enrichment of PLAGL family motif activity in ZR fusion tumour cells.

a, Workflow for mouse IUE tumour generation and preparation of snMultiome libraries and data. b, UMAP based on weighted nearest-neighbour analysis of integrated snMultiome data from mouse IUE tumours. EPN ZR (N = 3), GBM (N = 1) and EPN YM (N = 3) tumours generated by IUE. Tumour cells were identified by expression of established tumour marker genes. c, Cells from each tumour type projected on to integrated UMAP. d, Distribution of cells exhibiting tumour gene signatures specific to tumour type. e, Reconstructed UMAP based on tumour cells and annotated tumour cell types. f, Distribution of tumour cell types across individual tumour samples. g, Scatter plot illustrating tumour-type-specific motif differences relative to other tumour types. The x axis denotes the mean motif score, and the y axis represents the average log2 fold change (FC) in motif activity. Highly differential motifs are highlighted in red and labelled. h, Activity states of PLAG family motifs across all cell types, with tumour cell groups indicated. Max., maximum; min., minimum. i, PLAG family motif activity across cell types in tumour (ZR, YM, GBM) and non-tumour cell groups. OC, oligodendrocyte cell. j, Comparison of cell cycling signal score (y axis) with ZR fusion target gene expression signal score (x axis) across the various tumour cell types.

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