Maternal β-catenin and E-cadherin in mouse development

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 β-catenin gene from the mouse oocyte. Oocytes lacking E-cadherin, or expressing a truncated allele of β-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 β-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 β-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 β-catenin availability during embryonic genome activation.

Cell and molecular regulation of the mouse blastocyst

“…Loss of zygotic E-cadherin expression does not disrupt the initiation of compaction, probably owing to perdurance of maternally supplied E-Cadherin (Larue et al, 1994;Riethmacher et al, 1995). Maternal germline knockout of E-cadherin postpones compaction, but embryos are soon rescued by zygotic expression of the paternal allele (De Vries et al, 2004). Examination of loss of both maternal and paternal alleles of E-cadherin will be important for establishing the role of cell-cell contact in establishment of cell polarity.…”

Role of cadherins in health and in developing breast cancer

“…Этот процесс был впервые описан E. Hay в 1980 г. как центральный механизм раннего эмбрионального мор-фогенеза [22][23][24]. Потеря эпителиальной адгезии и по-лярности происходит во время формирования мезодермы и обеспечивает клеткам морфологию и свойства мезенхи-мальных клеток [25][26][27][28]. Первым этапом ЭМП является снижение экспрессии эпителиальных маркеров, таких как Е-кадгерин, за счет подавления транскрипции и уве-личение экспрессии мезенхимальных маркеров, таких как виментин [29][30][31].…”

Cytoplasmic Inheritance Redux

“…The cytoplasmic mRNA provides for a protein necessary prior to EGA, while the embryonic genome provides transcripts for the same protein-or isoforms of that protein-that are necessary post-EGA. An example of this is the cell adhesion protein E-cadherin, coded by the CDH-1 gene (De Vries et al, 2004). Knockout CDH-1 embryos develop to the blastocyst stage but fail to implant in the uterus.…”