Figure 7.

GLI^R upregulation compromises proliferation throughout the SVZ. A, Schematic diagram showing the dorsal (light gray) and ventral (dark gray) SVZ regions that were included in the analysis. Str, Striatum; Spt, septum; cc, corpus callosum; LV, lateral ventricle. B, C, Quantitative analysis of the number of KI67+ progenitors and LRCs per square centimeter in the dorsal (white bars) or ventral (gray bars) SVZ shows a significant decrease in the density of KI67+ progenitors in both regions of mGfap-Smo CKOs compared with Smo^lox/lox controls (Smo ctrl) that is more pronounced dorsally (B; n = 3 controls and 4 mutants; *p = 0.016, ****p < 0.0001; 2-way ANOVA with Sidak's post hoc test; mean ± SEM). A decrease in the density of the LRCs also was observed in the dorsal and ventral SVZ of mGfap-Smo CKOs compared with controls with no obvious change in the distribution between dorsal and ventral (C; n = 3 controls and 3 mutants). D–F, Dorsolateral SVZ sections stained for KI67 show a decrease in the number of KI67+ cells in the dorsal SVZ of mGfap-Smo CKOs when compared with controls (D, E), and a rescue of proliferation in the dorsal SVZ when Gli3 is ablated in mGfap-Smo CKOs (F). Scale bar: (in D) D–F, 50 μm. G, H, Quantitative analysis shows the recovery in the density of KI67+ progenitors and LRCs in mGfap-Gli3;Smo CKOs compared with controls (Gli3;Smo ctrl); as well as a similar distribution of KI67+ cells in the dorsal and ventral SVZ of mGfap-Gli2;Gli3 CKOs compared with controls (I) (Gli2;Gli3 ctrl; 2-way ANOVA with Sidak's post hoc test; mean ± SEM).