MAB-5 Hox expression in QL and its descendants specifies their posterior migration. UNC-40 and DPY-19 are required for initial QL posterior polarization (Honigberg and Kenyon, 2000), and a Wnt signal from the posterior induces
mab-5 expression in QL but not QR (Maloof, et al., 1999). MIG-15 is a Nck-interacting kinase that has been found to control Q neuroblast and descendant migration (E. Hedgecock) and to act with the Racs and integrin in axon pathfinding (Poinat, et al., 2002; Shakir, et al., 2006). Of Q descendants, the neurons AQR and PQR, generated from QR and QL, respectively, migrate to the most distal anterior and posterior locations (AQR in the head and PQR in the tail). In
mig-15 mutants, PQR was directed anteriorly instead of posteriorly, as seen for other QL descendants in
mab-5,
unc-40,
dpy-19, and wnt mutants. The constitutively-expressed
mab-5(
e1751) allele rescued the PQR directional migration defects in
mig-15 mutants, suggesting that MIG-15 acts upstream of MAB-5 and might be required for
mab-5 expression (Shakir, et al., 2006). MIG-15 might act with the Wnt pathway to control MAB-5 expression or with UNC-40 and DPY-19 to control the initial QL posterior polarity. In
unc-40,
dpy-19, and
bar-1(
ga80), a putative null state of Wnt signaling, AQR migration was largely normal, and misdirected PQR neurons migrated completely to the anterior to reside near AQR. In contrast, AQR and misdirected PQR neurons often failed to complete their anterior migrations in
mig-15 mutants (the stopping phenotype). The
mab-5(
e1239) null allele did not suppress the
mig-15 stopping phenotype, indicating that MIG-15 controls a MAB-5 independent process of cell migration. Interestingly, some wnt mutants that do not cause complete loss of Wnt signaling (due to hypomorphic alleles or redundant functions) also show a stopping phenotype in PQR but not AQR that is suppressed by the
mab-5(
e1239) null allele, suggesting that reactivation of
mab-5 in QL descendants can cause them to stall in their migration. The constitutive
mab-5(
e1751) allele caused PQR as well as AQR to migrate posteriorly in
mig-15 mutants. However, PQR and misdirected AQR often displayed stopping, a defect not seen in
mab-5(
e1751) alone. Together, these results suggest that MIG-15 acts upstream of MAB-5 to determine the direction of PQR migration but acts in a
mab-5-independent pathway to give AQR and PQR the ability to migrate fully to their proper locations.