Fig. 5
EGL size but not ML thickness recovers by P20. (a) Schematic of tissue orientation and quantification location. (b) ML thickness increases as the EGL area decreases during postnatal development in both control and Car8wdl mice. *** p < 0.001; **** p < 0.0001; One-way ANOVA; Tukey’s multiple comparisons post-hoc test; Mean ± SEM. (c-d) Both the ML thickness (n = 3 mutants, n = 5 controls) and EGL area (n = 8 mutants, n = 10 controls) are not significantly different between Car8wdl mutants and control mice at P5. ML thickness, p = 0.9631; EGL area, p = 0.8605; Student’s t-test; Mean ± SEM. (e-f) Both the ML thickness (n = 7 mutants, n = 6 controls) and EGL area (n = 10 mutants, n = 9 controls) are not significantly different between Car8wdl mutants and control mice at P10. ML thickness, p = 0.6896; EGL area, p = 0.1965; Student’s t-test; Mean ± SEM. (g-h) The EGL area (n = 10 mutants, n = 8 controls), but not ML thickness (n = 8 mutants, n = 6 controls) is significantly larger in P15 Car8wdl mutant mice compared to control mice. ML thickness, p = 0.8727; EGL area, * p < 0.05; Student’s t test; Mean ± SEM. (i-j) The EGL area in Car8wdl mutant mice (n = 9) normalizes to controls (n = 6), but its ML (n = 3 mutants, n = 4 controls) is now larger at P20. ML thickness, * p < 0.05; EGL area, p = 0.1211; Student’s t test; Mean ± SEM. The scale bar represents 50 μm