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  current news   Press   selected story    
     
  3 June 2016  
 
β-catenin-mediated adhesion is required for successful preimplantation mouse embryo development
 
 




Authors
Daniel Messerschmidt1,2,*, Wilhelmine N. de Vries3,*, Chanchao Lorthongpanich1,4, Sathish Balu1,5, Davor Solter 1,4 and Barbara B. Knowles1,2,4

1 Institute of Medical Biology, A*STAR, 8A Biomedical Grove, Immunos 06-06, 138648, Singapore.
2 Institute of Molecular and Cellular Biology, A*STAR, Proteos 5- 02, 138673, Singapore.
3 The Jackson Laboratory, 600 Main Street, Bar Harbor, ME 04609, USA.
4 Siriraj Center of Excellence for Stem Cell Research, Mahidol University, Bangkok, 10170 Thailand.
5 Nanyang Polytechnic, School of Chemical and Life Sciences, 569830, Singapore.
*These authors contributed equally to this work

Published in Development (2016) 143, 1993-1999 doi:10.1242/dev.133439 on May, 28th 2016

Abstract

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.

Figure::


Figure Legend:
The maternal-zygotic deletion βCatC results in an increased number of implantation sites. (A) Quantification of deciduomas isolated/uterus at 5.5, 6.5 and 7.5 dpc from females of the indicated mating schemes. (B) Thirty-one deciduomas isolated from a single uterus of a βCatCf/f;Zp3-Cre female mated with a βCatCΔ/+ male at 6.5 dpc. (C) Quantification of deciduomal content from all βCatCf/f;Zp3-Cre females mated with a βCatCΔ/+ male.

For more information on Daniel MESSERSCHMIDT's laboratory, please click here.