I. Rogers et S. Varmuza, LiCl disrupts axial development in mouse but does not act through the beta-catenin/Lef-1 pathway, MOL REPROD, 55(4), 2000, pp. 387-392
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.