Deletion of the Na/K-ATPase α1-subunit gene ( Atp1a1) does not prevent cavitation of the preimplantation mouse embryo

Abstract

Increases in Na/K-ATPase activity occur concurrently with the onset of cavitation and are associated with increases in Na +-pump subunit mRNA and protein expression. We have hypothesized that the α1-isozyme of the Na/K-ATPase is required to mediate blastocyst formation. We have tested this hypothesis by characterizing preimplantation development in mice with a targeted disruption of the Na/K-ATPase α1-subunit ( Atp1a1) using embryos acquired from matings between Atp1a1 heterozygous mice. Mouse embryos homozygous for a null mutation in the Na/K-ATPase α1-subunit gene are able to undergo compaction and cavitation. These findings demonstrate that trophectoderm transport mechanisms are maintained in the absence of the predominant isozyme of the Na +-pump that has previously been localized to the basolateral membranes of mammalian trophectoderm cells. The presence of multiple isoforms of Na/K-ATPase α- and β-subunits at the time of cavitation suggests that there may be a degree of genetic redundancy amongst isoforms of the catalytic α-subunit that allows blastocyst formation to progress in the absence of the α1-subunit.