Figure 3
EphA4 deletion to 50% at 60 days of age does not improve disease progression in the SOD1G93A mouse. (A–D) Disease progression was monitored in SOD1-EphA4het and SOD1-CAG-EphA4het mice, which received Tamoxifen at the age of 60 days (T60). (A) Performance decline in the hanging wire test (HW). (B) Median disease onset: 121.5 d (SOD1-EphA4het, N = 12) and 122 d (SOD1-CAG-EphA4het, N = 15), Log-rank p-value = 0.3867. (C) Median survival: 148 d (SOD1-EphA4het, N = 12) and 151 d (SOD1-CAG-EphA4het, N = 15), Log-rank p-value = 0.2892. (D) Average disease duration: 32.5 d ± 3.101 d (SOD1-EphA4het, N = 12) and 30.53 d ± 2.69 d (SOD1-CAG-EphA4het, N = 15), p-value = 0.6348. Two-way ANOVA test with repeated measurements was used to determine differences in the hanging wire performance decline, which is represented as mean ± SEM, whereas the Log-rank test was used for disease onset and survival. Disease progression was analysed with a two-tailed student t-test and represented as mean ± SEM. (E) EphA4 protein levels where reduced to about 50% in the lumbar spinal cord end-stage SOD1-CAG-EphA4het mice (N = 7–8) as measured by western blot and compared to EphA4 levels of SOD1-EphA4het mice. Representative cropped bands are shown and full-length western blots can be found in Supplementary Material. EphA4 C-terminal (EphA4 C-ter) antibody was used to quantify EphA4 levels and β-actin was used as a loading control. Data represents mean ± SEM, and different conditions were compared with a two-tailed t-test: ***P < 0.001.
