Faculty Advisor or Committee Member

Elizabeth F. Ryder, Advisor

Faculty Advisor or Committee Member

Joseph B. Duffy, Committee Member

Faculty Advisor or Committee Member

Jagan Srinivasan, Committee Member




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.


Worcester Polytechnic Institute

Degree Name



Biology & Biotechnology

Project Type


Date Accepted





C. elegans, ABI-1, MIG-10, Neuronal Migration