MIG-15 is a Nck-interacting kinase that has been found to act with the Racs and integrin in axon pathfinding (Poinat et al., 2002; Shakir et al., 2006). Hedgecock and Guo first described Q cell descendant migration defects in
mig-15 mutants. The bilateral Q neuroblasts, born between the V4 and V5 lateral seam cells, undergo initial anterior and posterior polarizations and migrations before dividing to produce neurons that will continue in their long-range anterior and posterior migrations. We found that mutations in
mig-15 reduced the size of the initial Q cell protrusions, but did not affect the direction of the initial polarizations. After this initial polarization at a time when in wild type the Q cells have migrated, the Q cells often fail to migrate and fail to maintain their initial proper polarizations, sending ectopic protrusions in both anterior and posterior directions. In order to examine the role of MIG-15 in the polarization and maintenance of polarization of the Q cells, we began looking at candidate genes that might be working with MIG-15 in these processes. Baum and Garriga (1997) showed that INA-1/a-integrin mutants have defects in Q cell descendant migration. Additionally, the C-terminus of MIG-15 has been shown to physically interact with the cytoplasmic domain of PAT-3/b-integrin (Poinat et al., 2002). Therefore, we began to examine the role of INA-1 in the Q cell polarization and maintenance of polarization. Analysis of the Q cells in
ina-1 null mutants showed that
mig-15 and
ina-1 mutants phenotypically resembled each other during the initial polarization stage, with both mutants containing Q cell protrusions that were reduced in size, but formed in the correct direction. Looking later at the migration stage when
mig-15 mutants fail to migrate and begin to send out ectopic protrusions,
ina-1 mutants also failed to migrate, but did not send out ectopic protrusions and remained polarized in the correct directions. Further analysis of the Q cell descendants displayed other similarities between
mig-15 and
ina-1 mutants, in which AQR and PQR both reversed directions of migration and failed to fully migrate along their normal migratory pathways. A double mutant of
mig-15 with
ina-1 resembled
ina-1 mutants alone for AQR/PQR migration, and overexpression of INA::GFP increased the AQR/PQR migratory defects in a hypomorphic
mig-15 background. Taken together, these results suggest that MIG-15 could be acting with integrin to regulate the polarization and migration of the Q cells and their descendants. In contrast, the maintenance of polarization appears to be independent of
ina-1, suggesting that MIG-15 might be working with other molecules to maintain the polarity of the Q cells.