Activation of β-catenin causes defects in embryonic development during maternal-to-zygotic transition in mice

The early stage of embryogenesis is an important and complex cell-remodeling event in reproductive biology. To develop into a normal zygote, maternal-to-zygotic transition (MZT) is especially important for both zygotic genome activation (ZGA) and degradation of maternal products during the early stage of embryonic development. beta-Catenin has been identified as an important regulator of embryonic development and adult stem cell division via the canonical Wnt/beta-catenin signalling pathway. However, the role of activated beta-catenin during MZT remains elusive. In the present study, we found that beta-catenin is mainly expressed during embryogenesis in the cell membrane from the zygote-to morula-stage embryos but not in MII oocytes. To analyze the function of activated beta-catenin during MZT, we conducted a beta-catenin activation assay during embryogenesis. Our results indicated that development beyond the two-cell stage was inhibited in zygotes with beta-catenin activation. Further analysis showed that activated form of beta-catenin protein was increased and the phosphorylated form of beta-catenin protein was decreased in culture embryos. Taken together, our study reveals that activation of beta-catenin may play a vital role in zygotic development, determining the developmental potential of mouse embryos.