β-Catenin Has Wnt-like Activity and Mimics the Nieuwkoop Signaling Center inXenopusDorsal–Ventral Patterning

Abstract

β-Catenin is a protein known to associate with the cytoplasmic domains of members of the cadherin family of cell adhesion molecules. Recently, Funayamaet al.(Funayamaet al.(1995).J. Cell Biol.128, 959–968.) demonstrated that overexpression of β-catenin causes the formation of a secondary axis inXenopus laevisembryos. In order to understand the role of β-catenin in axis formation, we examined its biological activity in further detail. β-Catenin is effective at inducing a secondary axis when overexpressed in the vegetal ventral region of early cleavage stage (4–32 cell) embryos. β-Catenin may act as part of the Nieuwkoop center because cells overexpressing β-catenin do not contribute directly to axial structures. Overexpression of β-catenin can specifyde novoaxis formation, as shown by its ability to rescue UV-ventralized embryos. Overexpression of β-catenin alone is not sufficient to cause elongation of animal caps or to induce mesodermal markers in animal caps. In these assays, overexpression of β-catenin behaves like ectopic expression of certain members of theWntgene family. Like Wnts, overexpression of β-catenin was also found to increase gap junctional communication in cells of the ventral animal cap. Overexpression of β-catenin causes a small increase in the rate of aggregation ofXenopusblastomeres. Overexpression of C-cadherin causes a more dramatic increase in the rate of aggregation ofXenopusblastomeres, but does not enhance gap junction communication or induce axis duplication; hence, we argue that increased adhesion is not sufficient to account for β-catenin's ability to regulate patterning or gap junction communication. We propose a signaling role for β-catenin during axis formation inXenopus.