Has a role in the Wnt signaling pathway controlling the asymmetry of cell divisions during embryogenesis (PubMed:10380924). Operates in the AB and EMS cell lineages influencing cell specification (PubMed:10391246). Required for body wall muscle development, endoderm development, pop-1 asymmetry and T-cell division asymmetry (PubMed:10380924, PubMed:9384382). Component of the beta-catenin-lit-1 complex which promotes the phosphorylation, down-regulation and subcellular relocation of pop-1 (PubMed:15066285, PubMed:10380924). Regulates plp-1 nuclear localization in embryos (PubMed:19084000). Plays a role in male tail tip morphogenesis (PubMed:21408209). ATP + L-seryl-[protein] = ADP + H(+) + O-phospho-L-seryl-[protein] ATP + L-threonyl-[protein] = ADP + H(+) + O-phospho-L-threonyl-[protein] Component of the beta-catenin-lit-1 complex (also called the lit-1/wrm-1 complex or the wrm-1/lit-1 kinase complex) at least composed of lit-1 and wrm-1 (PubMed:10380924, PubMed:15066285). Interacts with wrm-1 (via N-terminus); the interaction is direct and activates lit-1 kinase activity which leads to the phosphorylation of pop-1 (PubMed:10380924, PubMed:15066285). This promotes pop-1 interaction with par-5 and translocation of pop-1 from the nucleus to the cytoplasm (PubMed:15066285). Interacts with pop-1 (when phosphorylated on 'Ser-118' and 'Ser-127'); the interaction is dependent on the beta-catenin-lit-1 complex (PubMed:10380924, PubMed:15066285). Located in the anterior cell cortex before and during asymmetric cell division. After division, located preferentially in the nucleus of the posterior daughter cell. Localizes to the nucleus in hyp9 and hyp10 cells prior to male tail tip morphogenesis (PubMed:21408209). Expressed in the pharynx and seam and vulval cells. Expressed in the pharynx and seam and vulval cells in larvae (PubMed:15489294). Expressed in the male tail tip during the L4 larval stage (PubMed:21408209). Defects in body wall muscle, endoderm development and pop-1 asymmetry (PubMed:10380924, PubMed:10391246, PubMed:9384382). RNAi-mediated knockdown disrupts tail tip morphogenesis resulting in retention of the pointed larval tail tip in adult males (also known as the Lep phenotype) (PubMed:21408209). RNAi-mediated knockdown causes the transcription factor plp-1 to localize at much lower levels in nuclei and instead accumulate in the cytoplasm, during embryonic development. Belongs to the protein kinase superfamily. CMGC Ser/Thr protein kinase family. MAP kinase subfamily.