Fig. 3 | Nature Communications

Fig. 3

From: Atrx inactivation drives disease-defining phenotypes in glioma cells of origin through global epigenomic remodeling

Fig. 3

Atrx deficiency promotes mNPC motility. Transwell (a; 5 replicates) and wound healing (b, c; 3 replicates) assays showing increased migratory behavior in Atrx- mNPCs (scale bar 300 µm). This phenotype was accompanied by increased GTP-bound RhoA by IP western analysis (d) with quantitation by densitometry (e; average of 3 biological replicates, Vinculin loading control). f wound healing assay for Atrx+ and Atrx- NPCs treated with the RhoA inhibitor C3 exoenzyme at the designated levels (3 replicates; Atrx-: Veh vs 0.5 μg/ml—P = 0.034, Veh vs 1 μg/ml —P = 9.8 × 10-6, Veh vs 2 μg/ml —P = 5.5× 10-5; Atrx+: Veh vs 0.5 μg/ml—P = 8.5 × 10−11, Veh vs 1 μg/ml —P = 2.7 × 10−9, Veh vs 2 μg/ml —P = 1.4 × 10−9). P values determined by unpaired two-tailed t-test for both transwell assays and western blot densitometry, and by paired two-tailed t-test at all time points for wound healing assays