Despite the wealth of information surrounding axonal elongation and autophagy, it is still unclear why neuronal components shown to work at the level of axonal outgrowth and cytoskeleton stability bind to components of the autophagy machinery. Moreover, it is undetermined how the brain metabolite and neurotrophic agent Lanthionine ketimine (LK) promotes axonal outgrowth in unc-33 mutant nematodes. To shed light on the molecular players acting on axonal extension, we proceeded to study the effects of autophagy and LK on promoting axonal elongation. Based on previous work from our laboratory we hypothesized that axonal elongation defects observed in unc-33 mutants can be ameliorated by simultaneously inducing autophagy, a cellular recycling process, and treating nematodes with LKE (a cell-permeable ester form of LK). To test this hypothesis, we performed imaging analyses of fluorescently labeled axons of nematodes grown in the presence of LKE and possessing a temperature sensitive mutation that produces enhanced autophagy. Quantification of the prevalence of axonal abnormalities shows that autophagy induction significantly reduces the number of axons deformed by branching, bundling, and early terminations. Moreover, studies of LKE treatment demonstrated that the benefits of this treatment are additive to those of enhanced autophagy. Likewise, results of motility in liquid media also showed statistically significant differences between each of the experimental groups from the control, supporting that autophagy and LKE summate in their potential to rescue locomotion defects. Taken together, these results show that axonal outgrowth is directly or indirectly regulated by manipulating autophagy and the availability of LK.