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Fig. 8 | Neural Development

Fig. 8

From: Persistent motor dysfunction despite homeostatic rescue of cerebellar morphogenesis in the Car8 waddles mutant mouse

Fig. 8

Sox2 expression is upregulated in the P5 Car8wdl EGL. (A) Schematic of tissue orientation and quantification location. (B) Timeline detailing the experiment by delineating the times of the procedures performed over the course of 11 days. Two schematics are included to illustrate the method of EdU injections for P5 and P10 pups. (C,E) The number (no) of EdU-positive cells per 50 μm in lobules V/VI of Car8wdl tissue is comparable to that of controls at P5 and P10. The scale bars represent 500 μm (zoomed out) and 50 μm (zoomed in). In the graphs (E), the number of cells per 50 μm that are in interphase (i.e. S-phase) are not significantly different between Car8wdl and control cerebella at P5 (n = 6 controls, n = 4 mutants) or P10 (n = 5 controls, n = 5 mutants). P5, p = 0.0728; P10, p = 0.6245; Student’ t-test; Mean ± SEM. (D,F) Car8wdl mice (n = 3) have more Sox2-positive cells (yellow arrowheads) in the inner EGL compared to control mice (n = 3) at P5. By P10, Sox2-positive cells are predominantly localized to the PCL and immediately adjacent areas in the Car8wdl (n = 3) cerebellum like in the control cerebellum (n = 3). White dotted lines delineate the outer EGL (o). Magenta lines delineate the inner EGL (i). The scale bars represent 50 μm in (D). Quantification of the number (no) of Sox2+ cells in the P5 and P10 mutant and control inner EGL (~ 50% of the EGL, i.e. within ~ 27,000 μm2 or ~ 14,000 μm2 of the EGL) confirms the abundance of Sox2+ cells that were observed in the imaged tissue (F). P5, * p < 0.05; P10, p = 0.3739; Student’s t-test; Mean ± SEM

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