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Inhibition of the Beta-Catenin Signaling Pathway in Blastocyst and Uterus During the Window of Implantation in Mice¹

State Key Laboratory of Reproductive Biology,³ Institute of Zoology, Chinese Academy of Sciences, Beijing, 100080, China Graduate School of the Chinese Academy of Sciences,⁴ Beijing 100039, China Division of Reproductive Biology,⁵ Department of Obstetrics and Gynecology, Stanford University School of Medicine, Stanford, California 94305-5317

Beta-catenin, the mammalian homolog of Drosophila armadillo protein, was first identified as a cadherin-associated protein at cell-cell junctions. Another function of beta-catenin is the transduction of cytosolic signals to the nucleus in a variety of cellular contexts, which usually are elicited by the active form of beta-catenin. The aim of the present study was to examine the potential role of active beta-catenin in the mouse embryo and uterus during embryo implantation. Active beta-catenin was detected differentially in mouse embryos and uteri during the peri-implantation period. Aberrant activation of beta-catenin by LiCl, a well-known glycogen synthase kinase-3 inhibitor, significantly inhibited blastocyst hatching and subsequent adhesion and outgrowth on fibronectin. Results obtained from pseudopregnant and implantation-delayed mice imply an important role for implanting blastocysts in the temporal and spatial changes of active beta-catenin in the uterus during the window of implantation. Collectively, these results suggest that the beta-catenin signaling pathway is inhibited in both blastocyst and uterus during the window of implantation, which may represent a new mechanism to synchronize the development of preimplantation embryos and differentiation of the uterus during this process.

¹ Supported by the Special Funds for Major State Basic Research Project (G1999055903) and Funds from NSFC (30170112).

² Correspondence: En-Kui Duan, State Key Laboratory of Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing 100080, China. FAX: 86 10 62631831; duane{at}ioz.ac.cn

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