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

Citation
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
Citations number
35
Categorie Soggetti
Cell & Developmental Biology
Journal title
MOLECULAR REPRODUCTION AND DEVELOPMENT
ISSN journal
1040452X → ACNP
Volume
55
Issue
4
Year of publication
2000
Pages
387 - 392
Database
ISI
SICI code
1040-452X(200004)55:4<387:LDADIM>2.0.ZU;2-Z
Abstract
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.