To test if this defect could be recapitulated by expressing ALS mutant SOD1 in primary cultures of embryonic rat motor neurons we delivered EGFP, EGFP-SOD1 wild type (WT), A4V, G37R or G93A to DIV3 rat motor neurons by lentiviral transduction and analyzed axonal transport of MitoTracker Red CMXRos-labelled mitochondria from time-lapse recordings and corresponding kymographs as described by us before (Fig. 1A, a) (9,28,29). This evidence concerns the gene SOD1 and amyotrophic lateral sclerosis.