Figure 2
From: Sox9 is critical for suppression of neurogenesis but not initiation of gliogenesis in the cerebellum
En1-Cre and Pax2-Cre mediated inactivation of Sox9 in mouse cerebellum. (A and B) Conditional knockout of Sox9 driven by either En1-Cre or Pax2-Cre resulted in lethality at birth. Gross morphology of E18.5 embryos comparing the control and Sox9 mutants displayed. (C and D) H&E-stained cerebellar sagittal sections showing no alterations in morphological criteria of the cerebellum upon En1-Cre mediated Sox9 inactivation, despite efficient ablation of Sox9 expression in the mutant cerebellum as shown by the immunohistochemical staining detecting Sox9 indicated in (E and F). Strong expression of Sox9 could be observed in the control along the VZ at E15.5 while the mutant cerebellum lacked any Sox9 immunoreactivity. (G and H) Defect in cerebellar foliations was observed at E18.5 in the Pax2-Cre Sox9 mutant. (I and J) The fidelity of Pax2-Cre mediated Sox9 inactivation was validated by the complete absence of Sox9 expression in the mutant cerebellum. (K) Upon ablation of Sox9 using Pax2-Cre, no significant up-regulation of the closely related SoxE family member Sox10 transcript expression level was observed in the mutant using quantitative real-time PCR (p = 0.1617). The error bars indicate standard deviations. Abbreviations: vz, ventricular zone;. Scale bars: A and B: 1 cm; C-J: 100 μm.