Figure 5. Genetic ablation of Bax protects axons from degeneration in wl mice.

(A–D) Femoral nerves of mice of the indicated genotypes were examined at two months of age (genotypes above panels are for Atp8a2). The severe axonopathy in wl mutant mice (B), was significantly delayed by the Bax mutation (D). (E) Quantification of axon number in nerves from wl mutants either wild type or null for Bax (Bax^+/+ and Bax^−/− respectively) showed that Bax deficiency prevented the axon loss in wl/wl mutants. wl mice had significantly fewer axons than wild type control animals (420±12 axons versus 535±8). In contrast, wl mice that are Bax deficient do not have any axon loss compared to Bax deficient mice (note Bax deficient mice have more neurons because of lack of normal developmental neuronal death; Bax−/− 734±12 axons, wl/wl Bax ^−/− 731±9). Four mice of each genotype were examined. **, P = 0.01. Scale bar is 50 µm.