Regulation of blastocyst formation

Watson, Andrew J.; Barcroft, Lisa C.

doi:10.2741/watson

Cited by 154 publications

(122 citation statements)

References 217 publications

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“…There is evidence that IGF1 increases development to the blastocyst stage, at least in part, by regulating expression of genes involved in blastocoel formation. Blastocoel formation requires actions of ATP1A1 to increase blastocel fluid and facilitate tight junction formation [37,38] and IGF1 tended to increase expression of ATP1A1 in Day 7 blastocysts [22].…”

Section: Discussionmentioning

confidence: 99%

Timing and dependence upon mitogen-activated protein kinase signaling for pro-developmental actions of insulin-like growth factor 1 on the preimplantation bovine embryo

Bonilla

Ozawa

Hansen

2011

Growth Hormone & IGF Research

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Section: Discussionmentioning

confidence: 99%

Timing and dependence upon mitogen-activated protein kinase signaling for pro-developmental actions of insulin-like growth factor 1 on the preimplantation bovine embryo

Bonilla

Ozawa

Hansen

2011

Growth Hormone & IGF Research

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“…Poor expression of all the above genes in cytoplasmic hybrids may have adversely affected ICM and TE lineage segregation. The ion and fluid transport functions of the TE mediates the fluid dynamics that control cavitation and balstocyst formation (Watson & Barcroft 2001). The expression of Cdx2 is restricted to TE and is required for TE formation (Yamanaka et al 2006).…”

Section: Discussionmentioning

confidence: 99%

Nuclear–cytoplasmic incompatibility and inefficient development of pig–mouse cytoplasmic hybrid embryos

Amarnath

Choi²,

Moawad³

et al. 2011

Reproduction

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Inter-species somatic cell nuclear transfer (iSCNT) embryos usually fail to develop to the blastocyst stage and beyond due to incomplete reprogramming of donor cell. We evaluated whether using a karyoplast that would require less extensive reprogramming such as an embryonic blastomere or the meiotic spindle from metaphase II oocytes would provide additional insight into the development of iSCNT embryos. Our results showed that karyoplasts of embryonic or oocyte origin are no different from somatic cells; all iSCNT embryos, irrespective of karyoplast origin, were arrested during early development. We hypothesized that nuclear-cytoplasmic incompatibility could be another reason for failure of embryonic development from iSCNT. We used pig-mouse cytoplasmic hybrids as a model to address nuclear-cytoplasmic incompatibility in iSCNT embryos. Fertilized murine zygotes were reconstructed by fusing with porcine cytoplasts of varying cytoplasmic volumes (1/10 (small) and 1/5 (large) total volume of mouse zygote). The presence of pig cytoplasm significantly reduced the development of mouse zygotes to the blastocyst stage compared with control embryos at 120 h post-human chorionic gondotropin (41 vs 6 vs 94%, P!0.05; 1/10, 1/5, control respectively). While mitochondrial DNA copy numbers remained relatively unchanged, expression of several important genes namely Tfam, Polg, Polg2, Mfn2, Slc2a3 (Glut3), Slc2a1 (Glut1), Bcl2, Hspb1, Pou5f1 (Oct4), Nanog, Cdx2, Gata3, Tcfap2c, mt-Cox1 and mt-Cox2 was significantly reduced in cytoplasmic hybrids compared with control embryos. These results demonstrate that the presence of even a small amount of porcine cytoplasm is detrimental to murine embryo development and suggest that a range of factors are likely to contribute to the failure of inter-species nuclear transfer embryos.

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“…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).…”

Section: Introductionmentioning

confidence: 99%

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

Barcroft

Moseley

Lingrel

et al. 2004

Mechanisms of Development

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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 alpha1-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 alpha1-subunit (Atp1a1) using embryos acquired from matings between Atp1a1 heterozygous mice. Mouse embryos homozygous for a null mutation in the Na/K-ATPase alpha1-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 alpha- and beta-subunits at the time of cavitation suggests that there may be a degree of genetic redundancy amongst isoforms of the catalytic alpha-subunit that allows blastocyst formation to progress in the absence of the alpha1-subunit.

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Regulation of blastocyst formation

Cited by 154 publications

References 217 publications

Timing and dependence upon mitogen-activated protein kinase signaling for pro-developmental actions of insulin-like growth factor 1 on the preimplantation bovine embryo

Timing and dependence upon mitogen-activated protein kinase signaling for pro-developmental actions of insulin-like growth factor 1 on the preimplantation bovine embryo

Nuclear–cytoplasmic incompatibility and inefficient development of pig–mouse cytoplasmic hybrid embryos

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

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