LiCl disrupts axial development in mouse but does not act through the β-catenin/Lef-1 pathway
✍ Scribed by Ian Rogers; Sue Varmuza
- Publisher
- John Wiley and Sons
- Year
- 2000
- Tongue
- English
- Weight
- 187 KB
- Volume
- 55
- Category
- Article
- ISSN
- 1040-452X
No coin nor oath required. For personal study only.
✦ Synopsis
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 derived factors in the one-cell zygote. In our earlier study we used lithium chloride (LiCl) to perturb development of mouse axes.
Here we investigate whether the lithium induced axial defects in mouse are being mediated by the -catenin/ Lef-1 pathway as in Xenopus laevis. In lithium treated embryos we did not observe any changes in the amount or localization of -catenin protein. Furthermore, the lack of Lef-1 mRNA in treated and untreated embryos indicates the LiCl induced axial defects in the mouse are not mediated by the -catenin/Lef-1 pathway. Mol.