Receptor for Wnt proteins (PubMed:16930586, PubMed:22022276, PubMed:23295860, PubMed:24401370, PubMed:26292279). Most frizzled receptors are coupled to the beta-catenin canonical signaling pathway, which leads to the activation of disheveled proteins, inhibition of gsk-3 kinase, nuclear accumulation of beta-catenin and activation of Wnt target genes (Probable). A second signaling pathway involving PKC and calcium fluxes has been seen for some family members, but it is not yet clear if it represents a distinct pathway or if it can be integrated in the canonical pathway, as pkc seems to be required for Wnt-mediated inactivation of gsk-3 kinase (Probable). Both pathways seem to involve interactions with G-proteins (Probable). Required in embryonic development for the correct positioning and orientation of the mitotic spindles and division planes in blastomere cells (PubMed:9288749, PubMed:9288750, PubMed:20126385). During early embryonic cell divisions, directs the asymmetric positioning of transcription factors such as pop-1 and dsh-2 in daughter cells in order to determine cell fate specification (PubMed:12810601, PubMed:15620652, PubMed:15990090). Acts redundantly with other Wnt receptors such as lin-17 to control vulval precursor cell specification and also the polarity of different cell types including distal tip cells, seam cells, AVG interneurons and P-cells and their descendants (PubMed:16930586, PubMed:20126385, PubMed:22022276, PubMed:23295860, PubMed:24401370, PubMed:26292279). Plays a role in the migration of cell types including distal tip cells and the QR neuroblast descendants, QR.p and QR.pa during larval development (PubMed:20126385, PubMed:25373777, PubMed:26292279). Negatively regulates the unc-6/Netrin receptors unc-5 and unc-40 to control distal tip cell polarity and migration (PubMed:26292279). Acts through ced-5/DOCK180 and ced-10/Rac to control both distal tip cell migration and the phagocytic clearance of apoptotic cell corpses (PubMed:20126385). Furthermore, it is also required for the migration and axon guidance of the different neuronal cell types including CAN, ALM, HSN and the two mechanosensory neurons AVM and PVM (PubMed:16109397, PubMed:16516839, PubMed:25917219). Mediates Wnt receptor cfz-2 in directing ALM migration, but may also act redundantly with the Wnt receptors cfz-2 and mig-1 to direct the migration of other neuronal cell types including CAN and HSN (PubMed:16109397, PubMed:16516839). Mediates Wnt ligand egl-20 in the control of the anterior-posterior axon guidance of AVM and PVM neurons (PubMed:16516839). Uniformaly localized along the cell membrane throughout the cell cycle, but occasionally enriched at prophase towards the posterior pole of the cell (PubMed:15620652). Sequestered from the cell membrane to endosomes by plr-1 to prevent Wnt signaling (PubMed:24401370). Expressed in the 32-cell stage ABar blastomere and onwards into late embryogenesis (PubMed:15620652, PubMed:24401370). In late embryogenesis, enriched at the leading edges of postmitotic epidermal cells during ventral enclosure (PubMed:15620652). Asymmetrically expressed during the larval stages of development in cells of the gonad, vulva, tail, nervous system and hypodermis (PubMed:15620652). Expressed predominantly in QR neuroblast descendants and to a lesser extent in QL neuroblast descendants during the larval stages of development (PubMed:25373777). Expressed highly in anterior P-cells during larval development (PubMed:23295860). Post-embryonically, it is up-regulated at the transition phase after dorsal-ventral migration of distal tip cells and at the beginning of their anterior-posterior migration (PubMed:26292279). The FZ domain is involved in binding with Wnt ligands. Embryonic lethal with severely defective embryonic morphogenesis (PubMed:9288749, PubMed:9288750, PubMed:15620652). Embryos have defective mitotic spindle orientation in the 8-cell stage ABar blastomere (PubMed:9288749, PubMed:9288750, PubMed:20126385). Furthermore, there is disrupted asymmetric distribution of the transcription factor pop-1 and the disheveled homolog dsh-2, which are required for cell fate decisions in 8-cell stage ABar blastomeres and their descendants (PubMed:12810601, PubMed:15990090). There is also abnormal distal tip cell migration along the anterior-posterior axis of the body and defective clearance of apoptotic cell corpses in embryos (PubMed:20126385, PubMed:26292279). Both double knockout with unc-5 RNAi and knockdown by RNAi in an unc-40 mutant background suppresses the migratory defect of distal tip cells in the mom-5 and unc-40 single mutants (PubMed:26292279). Double knockout with Wnt receptor cfz-2 results in enhanced CAN neuron migration defects and also rescues the ALM migration defects in the single cfz-2 knockout (PubMed:16109397). Double knockout with Wnt receptor mig-1 results in enhanced HSN neuron migration defects and also in anterior-posterior axon guidance defects of PVM and AVM touch neurons (PubMed:16516839). RNAi-mediated knockdown results in embryonic lethality, but surviving animals display morphogenesis defects and PHA phasmid neuron duplication (PubMed:15990090). Belongs to the G-protein coupled receptor Fz/Smo family.