Fig. 2: ASCL1 and OLIG2 are required for tumor formation but inversely regulate different aspects of tumor migration in GBM mouse model. | Nature Communications

Fig. 2: ASCL1 and OLIG2 are required for tumor formation but inversely regulate different aspects of tumor migration in GBM mouse model.

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

Fig. 2: ASCL1 and OLIG2 are required for tumor formation but inversely regulate different aspects of tumor migration in GBM mouse model.

a Schematic showing induction of tdTOM+ brain tumors via electroporation of indicated Cre + CRISPR plasmids into neural progenitor cells in the right lateral ventricle of R26RT/T reporter mice at birth for longitudinal analyses. (b–q, s, t) Representative images of tdTOM+ tumors at P30, P60, or terminal stage in control (b–e), Ascl1-CKO (f–i), Olig2-CKO (j–m), and double CKO (n–q, s, t) mice (number of tumors imaged: n = 4/genotype for P30 & P60 and n = 6/genotype for terminal tumors). Arrows indicate midline and arrowheads mark the distance of migration of tdTOM+ tumor cells on the contralateral corpus callosum (CC). Asterisks demonstrate region imaged for (e, i, m, q, and t). ASCL1 and OLIG2 are highly co-expressed in control tdTOM+ tumor cells, but absent in the single or double CKO tdTOM+ tumors. Scale bars: 1 mm for whole brain sections; 25 μm for (e, i, m, q, t), and 12.5 μm for all insets. r Kaplan-Meier survival curves of each group of tumor mice showing statistical significance (Mantel-Cox test) between control versus experimental groups.

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