Neuronal and axonal migration are vital to the establishment of proper neuronal connections during development. The process of directed migration is dependent on reorganization of the actin cytoskeleton in response to external guidance cues. The MRL signaling proteins are thought to transmit positional information from surface guidance cues to the actin polymerization machinery, and thus to promote polarized outgrowth of axons during nervous system development (Quinn and Wadsworth, 2008). In C. elegans, mutations in the MRL family member
mig-10 result in animals that have defects in axon guidance, neuronal migration, and the outgrowth of the processes or 'canals' of the excretory cell, which is required for osmoregulation in the worm. To determine more of the molecular partners of MIG-10, we conducted a yeast two hybrid screen using isoform MIG-10A as bait. ABI-1, a downstream target of ABL non-receptor tyrosine kinase, was independently isolated 6 times as a strong MIG-10 interactor. ABI-1 is known to be part of the WAVE complex involved in the initiation of actin polymerization. Single mutants for
mig-10 and
abi-1 display similar phenotypes of incomplete migration of the ALM neurons and the excretory cell process. Furthermore,
abi-1(RNAi) enhanced the excretory canal truncation observed in
mig-10 mutants. Using both the yeast two-hybrid and a co-immunoprecipitation system, we are identifying domains within MIG-10 and ABI-1 that are necessary for their interaction. Our results suggest that MIG-10 and ABI-1 act together to link cell surface signaling with polarized actin polymerization.