Talk:Blastocyst Development

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Compaction

http://www.ncbi.nlm.nih.gov/pubmed/20042384

Compaction is initiated by E-cadherin mediated cell adhesion, which is regulated post-translationally via protein kinase C.

Gene replacement reveals a specific role for E-cadherin in the formation of a functional trophectoderm. Kan NG, Stemmler MP, Junghans D, Kanzler B, de Vries WN, Dominis M, Kemler R. Development. 2007 Jan;134(1):31-41. Epub 2006 Nov 30. PMID: 17138661

Phosphorylation of ezrin on threonine T567 plays a crucial role during compaction in the mouse early embryo. Dard N, Louvet-Vallée S, Santa-Maria A, Maro B. Dev Biol. 2004 Jul 1;271(1):87-97. PMID: 15196952


Expression of epithin in mouse preimplantation development: its functional role in compaction. Khang I, Sonn S, Park JH, Rhee K, Park D, Kim K. Dev Biol. 2005 May 1;281(1):134-44. PMID: 15848395

A targeted mutation in the mouse E-cadherin gene results in defective preimplantation development. Riethmacher D, Brinkmann V, Birchmeier C. Proc Natl Acad Sci U S A. 1995 Jan 31;92(3):855-9. PMID: 7846066


Zonula occludens-1 (ZO-1) is involved in morula to blastocyst transformation in the mouse. Wang H, Ding T, Brown N, Yamamoto Y, Prince LS, Reese J, Paria BC. Dev Biol. 2008 Jun 1;318(1):112-25. Epub 2008 Mar 20. PMID: 18423437

Regulation of blastocyst formation. Watson AJ, Barcroft LC. Front Biosci. 2001 May 1;6:D708-30. Review. PMID: 11333210

"Preimplantation or pre-attachment development encompasses the "free"-living period of mammalian embryogenesis, which directs development of the zygote through to the blastocyst stage. Blastocyst formation is essential for implantation, establishment of pregnancy and is a principal determinant of embryo quality prior to embryo transfer. Cavitation (blastocyst formation) is driven by the expression of specific sets of gene products that direct the acquisition of cell polarity within the trophectoderm, which is both the first epithelium of development and the outer cell layer encircling the inner cell mass of the blastocyst. Critical gene families controlling these events include: the E-cadherin-catenin cell adhesion family, the tight junction gene family, the Na/K-ATPase gene family and perhaps the aquaporin gene family. This review will update the roles of each of these gene families in trophectoderm differentiation and blastocyst formation. The current principal hypothesis under investigation is that blastocyst formation is mediated by a trans-trophectoderm ion gradient(s) established, in part, by Na/K-ATPase, which drives the movement of water through aquaporins (AQPs) across the epithelium into the extracellular space of the blastocyst to form the fluid-filled blastocoel. The trophectoderm tight junctional permeability seal regulates the leakage of blastocoel fluid, and also assists in the maintenance of a polarized Na/K-ATPase distribution to the basolateral plasma membrane domain of the mural trophectoderm. The cell-to-cell adhesion provided by the E-cadherin-catenin gene families is required for the establishment of the tight junction seal and the maintenance of the polarized Na/K-ATPase distribution. Blastocyst formation is therefore directly linked with trophectoderm cell differentiation, which arises through fundamental cell biological processes that are associated with the establishment of cell polarity."