Proper neuronal function requires a dynamic microtubule network and the directed movement of ATP dependent, cargo binding motor proteins: the mostly plus-end directed kinesins and minus end directed dyneins. The efficient coordination of both microtubules and motors is required for proper structure-function paradigms of neuronal signaling, the establishment of proper morphology during development and then the movement of vesicular cargo to facilitate proper synapse formation and subsequent signal transduction. Failure of neurons to perform any of these functions can lead to multitudes of disease pathologies, including those characterized as cognitive, degenerative, psychiatric, and developmental. The Kinesin-3 superfamily, consisting of C. elegans UNC-104, KLP-6, and KLP-4, are all neuronally expressed motor proteins that are evolutionarily conserved between worms and other higher eukaryotes. In vitro studies using mammalian homologues of these motors indicate that Kinesin-3 motors exhibit high affinity for microtubules and that these motors possess relatively long run lengths, thus are highly processive. This high degree of processivitiy has been hypothesized as an evolutionary adaptation for the movement of cargo over long distances, such as neuronal axons. Questions still remain as to the exact roles of these motor proteins in vivo; how they contribute to intracellular trafficking, protein stability, neuronal morphology, and signal transduction. To address these questions, we have begun a reverse genetic screen focusing on klp-4, the C. elegans homologue to human KIF13A and KIF13B. Using a combination of commercially available strains produced via large-scale mutagenesis and bioinformatics, we have identified a number potentially deleterious klp-4 alleles predicted to severely effect motor function. We are specifically interested in how mutation in KLP-4 may effect the paired AVB interneurons, which contain axons that extend the length the ventral nerve cord and are involved in the animal’s forward locomotive circuit and behaviors such as spontaneous reversals, social behavior, and the establishment of long term memory. We have determined that mutation in klp-4 does not appear to effect the development and gross morphology of the AVB interneuron, however different klp-4 mutant animals appear to have reduced response to nose touch suggesting role for KLP-4 in the establishment of proper distribution of subcellular components in neurons in vivo.