Cellular migration is an essential process for establishing neural connections during development. The MIG-10/RIAM/Lamellipodin signaling proteins are thought to send positional information from guidance cues to actin polymerization machinery, promoting the polarized outgrowth of axons. In C. elegans, mutations in the gene mig-10 result in the truncation of the migration of the mechanosensory neurons. Biochemical analysis demonstrates that MIG-10 interacts with abelson-interactor protein 1 (ABI-1), and therefore investigation into whether these proteins work together in the neuron to promote migration was completed. To demonstrate MIG-10 cell autonomy in the neuron, transgenic strains with specific expression of mig-10 were created. mig-10 mutants were rescued in the mechanosensory, anterior lateral microtubule neuron (ALM) by neuron specific expression of mig-10 but not by epithelial expression, suggesting that MIG-10 is acting cell autonomously. To determine ABI-1 cell autonomy, transgenic strains with specific neuronal expression of abi-1 were compared to the wild type strain. abi-1 mutants were rescued by neuron specific expression of abi-1 in the ALM, suggesting that ABI-1 also functions cell autonomously in the ALM during this migration. Further investigation into the MIG-10/ABI-1 relationship was done by feeding RNAi of abi-1 in a mig-10(ct41) mutant strain. The ALM migration was not more severely truncated in the double mutant, suggesting that MIG-10 and ABI-1 work in the same pathway. Taken together, this evidence supports a model where MIG-10 and ABI-1 work together autonomously within the ALM to promote migration.