Unattenuated GLI2R and GLI3R suppress adult SVZ neurogenesis. A, B, Quantitative analysis of the number of proliferating KI67+ progenitors, as well as LRCs in the SVZ of mGfap-Gli3;Smo CKOs show neurogenesis is no longer significantly reduced compared with controls (Gli3;Smo ctrl), indicating a rescue compared with mGfap-Smo CKOs (Fig. 3H). C–K, Cross sections of the RMS in control, mGfap-Smo CKOs, and mGfap-Gli3;Smo CKOs showing the specific increase in the cresyl violet-labeled, KI67+ and DCX+ migrating NB progenitors after Gli3 ablation in mGfap-Smo CKOs. Scale bar: (in C) C–K, 100 μm. L, No significant effect was observed on SVZ progenitor proliferation after ablation of all GLIA and GLIR function in mGfap-Gli2;Gli3 CKOs. M, Expression of a constitutive GLI3R isoform in the absence of GLIA in mGfap-Gli2;Gli3Δ699 CKOs causes a mild decrease in the number of SVZ progenitors compared with littermate controls (unpaired t test; mean ± SEM).