期刊
EXPERIMENTAL CELL RESEARCH
卷 314, 期 18, 页码 3356-3368出版社
ELSEVIER INC
DOI: 10.1016/j.yexcr.2008.08.021
关键词
Tight junction; ZO-2; ZO-1; Blastocyst; Trophectoderm; Epithelium; siRNA; Differentiation
资金
- BBSRC, UK [G18784]
- School of Biological Sciences, University of Southampton
- MRC [G0100558] Funding Source: UKRI
- Biotechnology and Biological Sciences Research Council [G18784] Funding Source: researchfish
- Medical Research Council [G0100558] Funding Source: researchfish
Apicolateral tight junctions (TJs) between epithelial cells are multiprotein complexes regulating membrane polarity and paracellular transport and also contribute to signalling pathways affecting cell proliferation and gene expression. ZO-2 and other ZO family members form a sub-membranous scaffold for binding TJ constituents. We investigated ZO-2 contribution to TJ biogenesis and function during trophectoderm epithelium differentiation in mouse preimplantation embryos. Out data indicate that ZO-2 is expressed from maternal and embryonic genomes with maternal ZO-2 protein associated with nuclei in zygotes and particularly early cleavage stages. Embryonic ZO-2 assembled at outer blastomere apicolateral junctional sites from the late 16-cell stage. junctional ZO-2 first co-localised with E-cadherin in a transient complex comprising adherens junction and TJ constituents before segregating to TJs after their separation from the blastocyst stage (32-cell onwards). ZO-2 siRNA microinjection into zygotes or 2-cell embryos resulted in specific knockdown of ZO-2 mRNA and protein within blastocysts. Embryos lacking ZO-2 protein at trophectoderm TJs exhibited delayed blastocoel cavity formation but underwent normal cell proliferation and outgrowth morphogenesis. Quantitative analysis of trophectoderm TJs in ZO-2-deficient embryos revealed increased assembly of ZO-1 but not occludin, indicating ZO protein redundancy as a compensatory mechanism contributing to the mild phenotype observed. In contrast, ZO-1 knockdown, or combined ZO-1 and ZO-2 knockdown, generated a more severe inhibition of blastocoel formation indicating distinct roles for ZO proteins in blastocyst morphogenesis. (c) 2008 Elsevier Inc. All rights reserved.
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