Maternal beta-catenin and E-cadherin in mouse development.

Document Type

Article

Publication Date

2004

Keywords

Animals, Blastomeres, Cadherins, Cell-Adhesion, Cell-Nucleus, Cytoskeletal-Proteins, Embryo, Female, Gene-Deletion, Gene-Expression, Genetic-Predisposition-to-Disease, Mice, Oocytes, Protein-Binding, Protein-Transport, Research-Support-Non-U, S, -Gov't, Research-Support-U, S, -Gov't-P, H, S, Trans-Activators

First Page

4435

Last Page

4445

JAX Source

Development 2004 Sep; 131(18):4435-45.

Abstract

The oocyte to embryo transition in metazoans depends on maternal proteins and transcripts to ensure the successful initiation of development, and the correct and timely activation of the embryonic genome. We conditionally eliminated the maternal gene encoding the cell adhesion molecule E-cadherin and partially eliminated the beta-catenin gene from the mouse oocyte. Oocytes lacking E-cadherin, or expressing a truncated allele of beta-catenin without the N-terminal part of the protein, give rise to embryos whose blastomeres do not adhere. Blastomere adhesion is restored after translation of protein from the wild-type paternal alleles: at the morula stage in embryos lacking maternal E-cadherin, and at the late four-cell stage in embryos expressing truncated beta-catenin. This suggests that adhesion per se is not essential in the early cleavage stage embryos, that embryos develop normally if compaction does not occur until the morula stage, and that the zona pellucida suffices to maintain blastomere proximity. Although maternal E-cadherin is not essential for the completion of the oocyte-to-embryo transition, absence of wild-type beta-catenin in oocytes does statistically compromise developmental success rates. This developmental deficit is alleviated by the simultaneous absence of maternal E-cadherin, suggesting that E-cadherin regulates nuclear beta-catenin availability during embryonic genome activation.

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