Figure 4
From: The RacGAP β-Chimaerin is essential for cerebellar granule cell migration
Arrested migration of GCs in Chn2 null animals. (a,b) Cerebellar BrdU pulse labeling at P10, collected at P35. BrdU+ cells accumulate in the ectopic clusters present in Chn2−/− mutants (white arrows). (c,d) Immunofluorescence for βgal and the glial cell marker GFAP, with DAPI as counterstain. The Bergmann Glial scaffold, which radially migrating GCPs adhere to during their migration from the iEGl to GCL, does not appear disrupted in Chn2−/− mutants. Of note, βgal immunoreactive cells may be seen collected on individual glial tracts (white arrowheads), suggesting some β-chimaerin deficient GCs may initiate but fail to complete radial migration. Insert shows a higher magnification view of the dotted area (green: βgal; red: GFAP). Scale bars, 50 μm. (e) Quantification of βgal+ cells arrested in the molecular layer of WT, Chn2+/− and Chn2−/− adult mice. One-way ANOVA, p = 1.1102e-16, n = 10. **p < 0.01, Tukey HSD test. Error bars represent SEM.
