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 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 beta-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-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 beta-catenin/Lef-1 pathway.
Rogers
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I
Department of Zoology, University of Toronto, Toronto, Canada.
Varmuza
S
S
D000818:Animals; D001755:Blastocyst / Q000378:metabolism; D019521:Body Patterning / Q000502:physiology*; D003598:Cytoskeletal Proteins / Q000378:metabolism*; D004268:DNA-Binding Proteins / Q000378:metabolism*; D005260:Female; D006064:Gonadotropins, Equine / Q000494:pharmacology; D007150:Immunohistochemistry; D007274:Injections, Intraperitoneal; D018021:Lithium Chloride / Q000494:pharmacology*; D051821:Lymphoid Enhancer-Binding Factor 1; D051379:Mice; D008815:Mice, Inbred Strains; D011247:Pregnancy; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013723:Teratogens / Q000494:pharmacology*; D015534:Trans-Activators; D014157:Transcription Factors / Q000378:metabolism*; D051176:beta Catenin
C495267:CTNNB1 protein, mouse; D003598:Cytoskeletal Proteins; D004268:DNA-Binding Proteins; D006064:Gonadotropins, Equine; C497574:Lef1 protein, mouse; D051821:Lymphoid Enhancer-Binding Factor 1; D013723:Teratogens; D015534:Trans-Activators; D014157:Transcription Factors; D051176:beta Catenin; D018021:Lithium Chloride