The QR and QL neuroblast descendants migrate long distances in opposite anterior-posterior directions to give rise to three neurons each. Investigations into Q cell migrations have revealed that MAB-5/Hox is a posterior migration determinant, as expression in the Q cells is necessary and sufficient to drive posterior migration, yet few positive transcriptional targets of MAB-5 have been found. Whole-animal RNA seq combined with functional analysis in Q migration revealed
spon-1/F-spondin as being positively regulated by MAB-5/Hox (Tamayo et al., 2013). SPON-1/F-spondin is a secreted molecule involved in cell adhesion of several tissues (Woo et al., 2008). Null or strong loss-of-function alleles of
spon-1 are lethal, and exhibit the paralyzed-at-two-fold (pat) due to improper muscle cell attachment.Here we show that MAB-5 non-autonomously regulates Q cell migrations through body-wall-muscle-specific activation of
spon-1 expression. We found that
spon-1 reduction partially suppressed posterior migrations driven by the constitutively-active gain-of-function
mab-5(
e1751) mutation. A Pspon-1::GFP transgene was expressed in specifically the posterior body-wall muscle cells at the time of Q migration, and was not expressed in the Q cells.
mab-5 is expressed in QL as well as other posterior cells including posterior body wall muscles. Pspon-1::GFP expression in body wall muscles increased as levels of MAB-5 were increased by
mab-5(
e1751) mutation and by transgenic expression of
mab-5 in body wall muscles, consistent with the RNA-seq results. Cell-specific RNAi suggested that
spon-1 was required in the tissues surrounding the Q cells, presumably body wall muscles, but not in the Q cells, suggesting a non-autonomous role for
mab-5 and
spon-1. We propose that MAB-5 activation of
spon-1 expression in posterior body wall muscle is required for proper Q migrations. Consistent with this model, hypomorphic viable mutations in
spon-1 displayed defects in QL and QR descendant migrations.Further genetic analysis found the posterior Hox genes
egl-5 and
lin-39 can act redundantly with
mab-5 in Q migrations. The role of
egl-5 in QR and QL is likely non-autonomous as
egl-5 is not expressed in either Q cell, and Q descendant migration defects were observed in double mutants with
mab-5 and in
egl-5 alone. Here we demonstrate a unique role where
lin-39,
mab-5, and
egl-5 all act in parallel to promote migration. Taken together, our results suggest that Hox genes can non-autonomously promote Q cell migration, and that MAB-5 patterns the posterior via
spon-1 expression to non-autonomously regulate Q migrations.