UNC-33 C. elegans hypomorph mutants exhibit inhibited axonal growth cone filopodial extension and premature termination. This leads to uncoordinated movement and decrease in overall motility. In our laboratory we are interested in finding means for rescuing unc-33 axonal defects and related motility deficiencies. We are investigating whether a secondary mutation producing an increase in autophagy will generate a correlated increase in axonal guidance and extension and facilitate motility in unc-33 mutants. We hypothesize the increase will have the desired effects, due to decrease in growth cone area and prematurely terminated axons that hinder appropriate neural function. To test this we are utilizing a temperature sensitive unc-33 mutant. This strain at NonPermissive Temperature (NPT) has induced increase in autophagy; and at the Permissive Temperature (PT) has basal levels of autophagy. Motility assay and growth cone areas were assessed in NPT and PT groups as well as wild type animals. Quantification of motility rates in liquid media suggests that increase in autophagy in the NPT mutants did in fact increase the animals' motility. Imaging assays also indicate a correlation between the increase in autophagy and rescue of the growth cone area. The analysis of the temperature sensitive mutant strain supports our working model and hypothesis.