During Caenorhabditis elegans development multiple cells migrate long distances or extend processes to reach their final position and/or to attain proper shape. These migrations/outgrowths are regulated by several signaling pathways. QL neuroblast descendants (QL.d) movements are an example of EGL-20/Wnt signaling-regulated migration. When Wnt signaling is disrupted QL.d migrate improperly and reach ectopic position in the worm's anterior. To identify new regulators of Wnt pathway we looked for enhancers of a weak retromer mutant
vps-29 QL.d migration defect. We identified serine/threonine kinase SEL-5/AAK1 as a strong enhancer of
vps-29 QL.d migration phenotype. AAK1 was previously shown to regulate Wnt signaling in Wnt receiving cells. However, our data assign SEL-5 requirement to the Wnt producing cells during QL.d migration. By GFP tagging of the endogenous
sel-5 locus we confirmed that
sel-5 is expressed in Wnt producing cells. Its role there is not yet clear but its function is not required for regulation of MIG-14/Wls level. Compound
sel-5 vps-29 mutants also display shortening of the posterior excretory canals. Interestingly this SEL-5 role seems to be distinct from the role in QL.d migration. Firstly, SEL-5 function is cell-autonomous in case of the excretory canal length, and secondly, mutations in Wnt pathway genes
lin-44/wnt,
lin-17/Frizzled and
mig-14/Wls lead to an excretory canal overgrowth instead of its shortening. We thus identified SEL-5 as both Wnt dependent and Wnt independent regulator of cell migration and cell growth in C.elegans.