Regulation of blastocyst formation

Deletion of the Na/K-ATPase $alpha;1-subunit gene (Atp1a1) does not prevent cavitation of the preimplantation mouse embryo

“…These findings demonstrate that trophectoderm transport mechanisms are maintained in the absence of the predominant isozyme of Na þ -pump localized in the basolateral membranes of mammalian trophectoderm cells (Benos, 1981;Watson and Kidder, 1988;Watson et al, 1990b;Waelchli et al, 1997;Betts et al, 1998;MacPhee et al, 2000). The observation that mammalian blastocysts express multiple isoforms of a-and b-subunits at the time of cavitation (reviewed by Watson and Barcroft, 2001;Kidder, 2002) suggests that there may be a degree of genetic redundancy amongst a-subunit isoforms that allows blastocyst formation to progress in the absence of the a1-isoform. It is clear, however, that continued expression of the a1/b-isozyme of the Na/K-ATPase is required to support mammalian development beyond the preimplantation phase of development.…”

“…Blastocyst formation (cavitation) is dependent on formation of the trophectoderm epithelium, and is initiated following the establishment of ion gradients and osmotic fluid accumulation across this cell layer (reviewed by Borland, 1977;Wiley, 1984;Biggers et al, 1988;Benos and Balaban, 1990;Watson, 1992;Watson et al, 1999;Watson and Barcroft, 2001). Transporting epithelia utilize the polarized localization of ion transporters and channels within apical and basolateral membrane domains to establish and maintain trans-cellular ion gradients necessary for ion and solute transport, energized by basolateral expression of the Na þ and K þ adenosine triphosphatase (Na/K-ATPase).…”

“…Increases in Na/K-ATPase activity occur concurrently with the onset of cavitation Tupper, 1975, 1977;Dumoulin et al, 1993;Betts et al, 1998) and are associated with increases in Na þ -pump subunit mRNA (Gardiner et al, 1990;Watson et al, 1990b;Betts et al, 1997) and protein expression (Benos, 1981;Watson and Kidder, 1988;Overstrom et al, 1989;Gardiner et al, 1990). Multiple isoforms of a-and b-subunits (as many as six isozymes) are expressed by murine (Watson and Kidder, 1988;Betts et al, 1997Betts et al, , 1998Jones et al, 1997;Waelchli et al, 1997;MacPhee et al, 2000;Barcroft et al, 2002;Jones et al, 2001 reviewed by Watson and Barcroft, 2001;Kidder, 2002) and bovine (Betts et al, 1997(Betts et al, , 1998 preimplantation embryos. The a1-subunit, however, appears to be the predominant isoform expressed within the basolateral membranes of the trophectoderm in all species examined (Watson and Kidder, 1988;Betts et al, 1998;MacPhee et al, 2000;Waelchli et al, 1997).…”

Importance of Methionine Metabolism in Morula-to-blastocyst Transition in Bovine Preimplantation Embryos

“…However, apart from the fact that the roles of TEAD4 in ICM/TE lineage segregation have not been elucidated in bovine species, it is possible that abnormally high expression of TEAD4 in the ethionine-treated morula hampers ordered cell differentiation, thus impairing blastocyst formation. In addition, blastocyst formation is driven not only by cell lineage specification but also by fluid accumulation within embryos to form the blastocoelic cavity [35,36]. Na+ and K+ transporter (Na/K-ATPase) and water channels (aquaporins) are thought to be involved in the cavitation [35].…”

The optimal timing of blastocyst vitrification after trophectoderm biopsy of preimplantation genetic screening

“…Actually, TE biopsy appears to cause the rupture of the TJs between TE cells, which are responsible for paracellular sealing for retaining Na + and water molecules inside the blastocoel [15]. The TJs between TE cells play a crucial role in intercellular integrity, embryo amino acid turnover [15,30], embryonic growth [31] and implantation [32]. The paracellular sealing and sodium pump (Na+/K +-ATPase) facilitates gradually increasing fluid accumulation in the blastocoel [16], resulting in increased pressure on both the TE and ZP to increase blastocoel size to form an expanded blastocyst.…”