mig-15 encodes the C. elegans ortholog of vertebrate Nck-interacting kinase (NIK) which belongs to the STE20/germinal center kinase (GCK) family; MIG-15 is required for normal axon pathfinding, and to inhibit premature branching of commissures; RNAi of mig-15 and pat-3, which encodes a beta1A integrins, results in similar axonal defects, and mutations in ina-1, which encodes an alpha integrin chain, enhances the commissural phenotype of mig-15 mutations; MIG-15 also regulates multiple aspects Q cell behavior, including initial Q cell polarization (direction of lamellipodium extension) and maintenance of that polarity, as well as migration of the Q cells and their descendants; genetic mosaic analyses indicate that MIG-15 likely acts cell autonomously at least in AQR and PQR to regulate their migration; MIG-15 physically interacts with the cytoplasmic domain of the beta1A integrin, PAT-3; loss of mig-15 results in increased synapse number and synaptic tiling defect in DA neurons.
Predicted to enable protein serine/threonine kinase activity. Involved in several processes, including dorsal/ventral axon guidance; nematode larval development; and regulation of GABAergic synaptic transmission. Predicted to be located in cytoplasm. Expressed in several structures, including QL; QR; body wall musculature; pharynx; and somatic nervous system. Used to study epilepsy. Human ortholog(s) of this gene implicated in several diseases, including autosomal recessive intellectual developmental disorder 54; gastrointestinal system cancer (multiple); and hepatitis B. Is an ortholog of human MAP4K4 (mitogen-activated protein kinase kinase kinase kinase 4); MINK1 (misshapen like kinase 1); and TNIK (TRAF2 and NCK interacting kinase).