Rescue of axonal length defects by the addition of human wild-type TUBA4A mRNA. Zebrafish embryos were injected with an ATG morpholino against zebrafish tuba8l2 (0.160 mM) with or without the injection of human wild-type TUBA4A mRNA (300 ng/μl). Non-injected embryos were also included in the analysis. (a) Representative whole body images of zebrafish embryos for the different conditions at 48 hpf (scale bar represents 500 μm). (b) At 30 hpf, axonal length was measured for all conditions, with p = 0.0051 (AMO 0.160 mM versus AMO 0.160 mM + TUBA4A mRNA), p < 0.0001 (AMO 0.160 mM versus non-injected) and p < 0.0001 (non-injected versus AMO 0.160 mM + TUBA4A mRNA); one-way ANOVA with Dunnett’s multiple comparisons. Axonal length was measured for N = 3 experiments; n = 10–15 zebrafish per group per experiment; with every data point representing the average length of the five measured axons for each zebrafish embryo. **p < 0.01; ****p < 0.0001. AMO, morpholino; hpf, hours post fertilization.
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