Publication: Β-catenin-mediated adhesion is required for successful preimplantation mouse embryo development
Issued Date
2016-06-01
Resource Type
ISSN
14779129
09501991
09501991
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2-s2.0-84973519398
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Mahidol University
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SCOPUS
Bibliographic Citation
Development (Cambridge). Vol.143, No.11 (2016), 1993-1999
Suggested Citation
Daniel Messerschmidt, Wilhelmine N. De Vries, Chanchao Lorthongpanich, Sathish Balu, Davor Solter, Barbara B. Knowles Β-catenin-mediated adhesion is required for successful preimplantation mouse embryo development. Development (Cambridge). Vol.143, No.11 (2016), 1993-1999. doi:10.1242/dev.133439 Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/43036
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Title
Β-catenin-mediated adhesion is required for successful preimplantation mouse embryo development
Abstract
© 2016. Published by The Company of Biologists Ltd. β-catenin (CTNNB1) is integral to cell adhesion and to the canonical Wnt signaling pathway. The effects of maternal and zygotic CTNNB1 on embryogenesis have each been separately assessed, whereas the effect of its total absence has not. As the ‘traditional’ conditional Ctnnb1 knockout alleles give rise to truncated CTNNB1 fragments, we designed a new knockout allele incapable of CTNNB1 production. Mouse embryos lacking intact maternal/zygotic CTNNB1 from two knockout strains were examined in detail. Preimplantation embryos are formed, yet abnormalities in their size and shape were found throughout pre- and early postimplantation development. In the absence of the zona pellucida, embryos lacking CTNNB1 undergo fission and these separated blastomeres can become small trophoblastic vesicles, which in turn induce decidual reactions. Comparing the severity of this defective adhesion phenotype in embryos bearing the null allele with those carrying the ‘traditional’ knockout allele suggests a hypomorphic effect of the truncated CTNNB1 protein fragment, an important observation with possible impact on previous and future studies.