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Significance p120-catenin, an armadillo-repeat protein, regulates the stability of classical cadherins, but its cellular functions in vivo remain unclear. Here, we show that genetic deletion ofp120-catenin in the mouse embryo causes developmental arrest at midgestation with a bifurcation of the posterior body axis. This morphological defect is associated with an expanded primitive streak, p53-dependent cell death, and abnormal mesoderm migration. The expanded primitive streak inp120-catenin mutants is caused by ectopic activation of the canonical WNT signaling pathway, and the bifurcation of the axis is associated with accumulation of mesoderm cells that migrate without direction. The functions of p120-catenin in the early mouse embryo are likely to be important during other developmental epithelial-to-mesenchymal transitions (EMTs) and in tumor metastasis.

p120-catenin regulates WNT signaling and EMT in the mouse embryo