LiCl disrupts axial development in mouse but does not act through the beta-catenin/Lef-1 pathway

Chimera and cell marking studies suggest that axial determination in mouse embryos occurs at postimplantation stages. In contrast, Xenopus laevis axes are determined early due to the asymmetric distribution of maternally deri ved factors in the one-cell zygote. In our earlier study we used lithium ch loride (LiCl) to perturb development of mouse axes. Here we investigate whe ther the lithium induced axial defects in mouse are being mediated by the b eta-catenin/Lef-1 pathway as in Xenopus laevis. In lithium treated embryos we did not observe any changes in the amount or localization of beta-cateni n protein. Furthermore, the lack of Lef-1 mRNA in treated and untreated emb ryos indicates the LiCl induced axial defects in the mouse are not mediated by the beta-catenin/Lef-1 pathway. Mol. Reprod. Dev. 55:387-392, 2000. (C) 2000 Wiley-Liss, Inc.