Asymmetric cell division contributes to cell diversity in embryos and the maintenance of various stem cells, and hence, is critical for making multicellular organisms. Asymmetric cell division requires cellular polarization which is often regulated by extracellular signals including Wnt proteins. However, exact roles of Wnts in cell polarity remain elusive. In C. elegans the mid-stage embryo, blastomeres stereotypically and sequentially divide along the anterior-posterior axis. During the divisions, TCF/POP-1 protein, the downstream transcription factor of the Wnt pathway, accumulates higher in the anterior than the posterior daughter cell nuclei. The polarization in these asymmetric divisions occurs globally, including the blastomeres far from the Wnt source cells. Although the previous study using isolated blastomeres shows the involvement of the Wnt ligand, MOM-2, and the Frizzled type receptor, MOM-5 in establishing POP-1 polarity (Park & Priess 2003). Since
mom-2 and
mom-5 intact embryos show normal POP-1 polarity, however, their roles in mid-stage embryos are not clear. In this study, we found the POP-1 polarity was not established in the
mom-5 null mutant with the simultaneous knocking down of CAM-1 that is the ROR type Wnt receptor. Further, we performed the precise deletion of the Wnt-binding domain (CRD) of MOM-5 by genome editing. In the
cam-1 mutant lacking CRD of MOM-5, we found that polarity orientation is randomized, unlike double receptor-deficient embryo that shows loss-of polarity. The results suggest that the intracellular domain of
mom-5 facilitates the establishment of the polarity, and the Wnt ligands control polarity orientation. We will discuss how the Wnt receptors establish the cell polarity by interaction with the ligands in the mid-stage embryo.