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First published online 3 November 2004
doi: 10.1242/dev.01458
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1 Max-Planck Institute of Immunobiology, Stuebeweg 51, 79108 Freiburg,
Germany
2 Department of Pharmacology, Kyoto University Graduate School of Medicine,
Yoshida-Konoé-cho, Sakyo-ku, Kyoto, 606-8501, Japan
3 The Jackson Laboratory, Bar Harbor, ME 04609-1500, USA
* Author for correspondence (e-mail: kemler{at}immunbio.mpg.de)
Accepted 22 September 2004
Many components of the Wnt/ß-catenin signaling pathway are expressed during mouse pre-implantation embryo development, suggesting that this pathway may control cell proliferation and differentiation at this time. We find no evidence for a functional activity of this pathway in cleavage-stage embryos using the Wnt-reporter line, BAT-gal. To further probe the activity of this pathway, we activated ß-catenin signaling by mating a zona pellucida3-cre (Zp3-cre) transgenic mouse line with a mouse line containing an exon3-floxed ß-catenin allele. The result is expression of a stabilized form of ß-catenin, resistant to degradation by the GSK3ß-mediated proteasome pathway, expressed in the developing oocyte and in each cell of the resulting embryos. Nuclear localization and signaling function of ß-catenin were not observed in cleavage-stage embryos derived from these oocytes. These results indicate that in pre-implantation embryos, molecular mechanisms independent of the GSK3ß-mediated ubiquitination and proteasome degradation pathway inhibit the nuclear function of ß-catenin. Although the mutant blastocysts initially developed normally, they then exhibited a specific phenotype in the embryonic ectoderm layer of early post-implantation embryos. We show a nuclear function of ß-catenin in the mutant epiblast that leads to activation of Wnt/ß-catenin target genes. As a consequence, cells of the embryonic ectoderm change their fate, resulting in a premature epithelial-mesenchymal transition.
Key words: Epithelial-mesenchymal transition, Mouse pre-implantation embryo, Wnt/ß-Catenin, Gastrulation
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