In C. elegans Wnt signaling pathways control cell polarity during embryonic and postembryonic development. In the early C. elegans embryo Wnt signaling controls the polarity of the EMS blastomere. MOM-2 is a Wnt signal produced in the four-cell embryo by the P2 blastomere, which polarizes the EMS blastomere and thereby confers distinct fates on the EMS daughters: E, which gives rise to endoderm, and MS, which gives rise to mesoderm (Rocheleau, et al., 1997; Thorpe, et al., 1997). Other components of the Wnt pathway also function in this process, including MOM-1 (Porcupine), MOM-5, (Frizzled) and WRM-1 (-catenin). However, mutations affecting the transcription factor POP-1 (TCF) cause the opposite phenotype, suggesting that it represses signal transduction in the absence of Wnt signaling (Lin, et al., 1995). The level of POP-1 has been shown to be higher in the anterior MS cell than it is in the posterior E cell, suggesting that Wnt signaling functions to down-regulate POP-1 levels in E, allowing Wnt-induced gene expression (Lin, et al., 1998). Wnt signaling also controls cell polarities of the B and T (both TL and TR) cells in developing larvae. A Wnt protein encoded by
lin-44 is expressed in the tail hypodermal cells and affects the polarity of the asymmetric cell divisions of the more anterior T and B cells (Herman, et al., 1995). Mutations in
lin-17, which encodes a Frizzled related-protein (Sawa, et al., 1996) cause a loss of cell polarity in the B and T cells (Sternberg and Horvitz, 1988), suggesting that LIN-17 may be the receptor for LIN-44 signal. No other C. elegans homologs of Wnt pathway components are known to affect the polarities of the B and T cells.