Please use this identifier to cite or link to this item: https://doi.org/10.1371/journal.pone.0099532
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dc.titleZO-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
dc.contributor.authorPhua D.C.Y.
dc.contributor.authorXu J.
dc.contributor.authorAli S.M.
dc.contributor.authorBoey A.
dc.contributor.authorGounko N.V.
dc.contributor.authorHunziker W.
dc.date.accessioned2019-11-05T00:36:26Z
dc.date.available2019-11-05T00:36:26Z
dc.date.issued2014
dc.identifier.citationPhua 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
dc.identifier.issn1932-6203
dc.identifier.urihttps://scholarbank.nus.edu.sg/handle/10635/161406
dc.description.abstractThe 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.
dc.rightsAttribution 4.0 International
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.sourceUnpaywall 20191101
dc.subjectezrin
dc.subjectpodocalyxin
dc.subjectprotein ZO1
dc.subjectprotein ZO2
dc.subjectpodocan protein, mouse
dc.subjectprotein
dc.subjectprotein ZO1
dc.subjectprotein ZO2
dc.subjectTjp1 protein, mouse
dc.subjectTjp2 protein, mouse
dc.subjectanimal cell
dc.subjectapical membrane
dc.subjectarticle
dc.subjectbasement membrane
dc.subjectcavity formation
dc.subjectcontrolled study
dc.subjectectoderm
dc.subjectembryo
dc.subjectembryo development
dc.subjectembryoid body
dc.subjectembryonic stem cell
dc.subjectendoderm
dc.subjectepithelium cell
dc.subjectin vitro study
dc.subjectmicrovillus
dc.subjectmorphogenesis
dc.subjectmouse
dc.subjectnonhuman
dc.subjectprotein expression
dc.subjectprotein function
dc.subjectprotein localization
dc.subjectsurvival rate
dc.subjecttight junction
dc.subjectanimal
dc.subjectcytology
dc.subjectectoderm
dc.subjectembryoid body
dc.subjectembryonic stem cell
dc.subjectendoderm
dc.subjectgene expression regulation
dc.subjectgenetics
dc.subjectknockout mouse
dc.subjectmetabolism
dc.subjectAnimals
dc.subjectEctoderm
dc.subjectEmbryoid Bodies
dc.subjectEmbryonic Stem Cells
dc.subjectEndoderm
dc.subjectGene Expression Regulation, Developmental
dc.subjectMice
dc.subjectMice, Knockout
dc.subjectProteins
dc.subjectZonula Occludens-1 Protein
dc.subjectZonula Occludens-2 Protein
dc.typeArticle
dc.contributor.departmentDEPT OF PHYSIOLOGY
dc.description.doi10.1371/journal.pone.0099532
dc.description.sourcetitlePLoS ONE
dc.description.volume9
dc.description.issue6
dc.description.pagee99532
dc.published.statePublished
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