Please use this identifier to cite or link to this item: https://doi.org/10.1371/journal.pone.0099532
Title: ZO-1 and ZO-2 are required for extra-embryonic endoderm integrity, primitive ectoderm survival and normal cavitation in embryoid bodies derived from mouse embryonic stem cells
Authors: Phua D.C.Y.
Xu J.
Ali S.M.
Boey A.
Gounko N.V.
Hunziker W. 
Keywords: ezrin
podocalyxin
protein ZO1
protein ZO2
podocan protein, mouse
protein
protein ZO1
protein ZO2
Tjp1 protein, mouse
Tjp2 protein, mouse
animal cell
apical membrane
article
basement membrane
cavity formation
controlled study
ectoderm
embryo
embryo development
embryoid body
embryonic stem cell
endoderm
epithelium cell
in vitro study
microvillus
morphogenesis
mouse
nonhuman
protein expression
protein function
protein localization
survival rate
tight junction
animal
cytology
ectoderm
embryoid body
embryonic stem cell
endoderm
gene expression regulation
genetics
knockout mouse
metabolism
Animals
Ectoderm
Embryoid Bodies
Embryonic Stem Cells
Endoderm
Gene Expression Regulation, Developmental
Mice
Mice, Knockout
Proteins
Zonula Occludens-1 Protein
Zonula Occludens-2 Protein
Issue Date: 2014
Citation: Phua D.C.Y., Xu J., Ali S.M., Boey A., Gounko N.V., Hunziker W. (2014). ZO-1 and ZO-2 are required for extra-embryonic endoderm integrity, primitive ectoderm survival and normal cavitation in embryoid bodies derived from mouse embryonic stem cells. PLoS ONE 9 (6) : e99532. ScholarBank@NUS Repository. https://doi.org/10.1371/journal.pone.0099532
Rights: Attribution 4.0 International
Abstract: The Zonula Occludens proteins ZO-1 and ZO-2 are cell-cell junction-associated adaptor proteins that are essential for the structural and regulatory functions of tight junctions in epithelial cells and their absence leads to early embryonic lethality in mouse models. Here, we use the embryoid body, an in vitro peri-implantation mouse embryogenesis model, to elucidate and dissect the roles ZO-1 and ZO-2 play in epithelial morphogenesis and de novo tight junction assembly. Through the generation of individual or combined ZO-1 and ZO-2 null embryoid bodies, we show that their dual deletion prevents tight junction formation, resulting in the disorganization and compromised barrier function of embryoid body epithelial layers. The disorganization is associated with poor microvilli development, fragmented basement membrane deposition and impaired cavity formation, all of which are key epithelial tissue morphogenetic processes. Expression of Podocalyxin, which positively regulates the formation of microvilli and the apical membrane, is repressed in embryoid bodies lacking both ZO-1 and ZO-2 and this correlates with an aberrant submembranous localization of Ezrin. The null embryoid bodies thus give an insight into how the two ZO proteins influence early mouse embryogenesis and possible mechanisms underlying the embryonic lethal phenotype. © 2014 Phua et al.
Source Title: PLoS ONE
URI: https://scholarbank.nus.edu.sg/handle/10635/161406
ISSN: 1932-6203
DOI: 10.1371/journal.pone.0099532
Rights: Attribution 4.0 International
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