Fig. 7: Ascl1 overexpression promotes NSC/astroglial-like cells and suppresses OPC/oligodendroglial-like cells in mouse GBMs. | Nature Communications

Fig. 7: Ascl1 overexpression promotes NSC/astroglial-like cells and suppresses OPC/oligodendroglial-like cells in mouse GBMs.

From: Transcription factors ASCL1 and OLIG2 drive glioblastoma initiation and co-regulate tumor cell types and migration

Fig. 7: Ascl1 overexpression promotes NSC/astroglial-like cells and suppresses OPC/oligodendroglial-like cells in mouse GBMs.

af UMAPs demonstrating the proportion and distribution of 7 assigned cell types in control (ac) and Ascl1-OE (df) tumors based on cell type-specific gene signatures. g, h Differential gene expression confirms downregulation of oligodendrocyte lineage-specific genes (g) and upregulation of NSC/astrocyte-specific genes (h) in Ascl1-OE tumor cells. Bar graphs are mean Log2 Fold Change ± SEM for indicated genes by comparing cell type x cell type between control and Ascl1-OE tumors. Open circles within each bar graph represent number of cell types with indicated genes significantly altered (adjusted p-value < 0.05). Note that MOL genes are mostly restricted to MOL and thus only downregulated in that cell type. i Heatmap of averaged transcriptome for each assigned cell type into unionized RNA-seq triplicates (columns) for control and Ascl1-OE tumors showing specificity of signature genes (rows) to their respective cell types (black rectangles). Note that all cell types of control tumors expressed some level of OPC signature genes, which were the most drastically downregulated in Ascl1-OE tumors followed by NFOL and MOL signature genes (blue arrows), while NSC and astrocyte signature genes were highly upregulated across all cell types in Ascl1-OE tumors (red arrows).

Back to article page