Tight junction protein ZO-2 expression and relative function of ZO-1 and ZO-2 during mouse blastocyst formation

Sheth, Bhavwanti; Nowak, Rachael L.; Anderson, Rebecca G.; Kwong, Wing Yee; Papenbrock, Thomas; Fleming, Tom P.

doi:10.1016/j.yexcr.2008.08.021

Cited by 40 publications

(43 citation statements)

References 45 publications

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“…These investigations have implicated both, ZO-1 and ZO-2, as vital regulators of TJ strand formation and paracellular transepithelial transport [16] [17]. Such findings may explain the mechanism behind the developmental arrest of ZO-1 depleted mouse morula [51] or the delayed blastocyst morphogenesis of ZO-1 and/or ZO-2 depleted mouse embryos [52]. These in vitro studies on morula-blastocyst development, and the study on self-renewal and differentiation of ZO-1 -/- mouse embryonic stem cells [26], point to the significance of the ZO proteins in early mammalian embryogenesis.…”

Section: Discussionmentioning

confidence: 95%

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

Phua

Ali

et al. 2014

PLoS ONE

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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.

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Section: Discussionmentioning

confidence: 95%

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

Phua

Ali

et al. 2014

PLoS ONE

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“…The TJ is essential for paracellular sealing of the outer cells as they undergo epithelialization to generate the blastocyst cavity [42,43,47,48]. The involvement of PAR6 homologs in TJ formation has been investigated in mammalian cultured epithelial cells, in which epithelium formation is experimentally induced after the disruption of cell-cell contacts.…”

Section: Discussionmentioning

confidence: 99%

Cell Polarity Regulator PARD6B Is Essential for Trophectoderm Formation in the Preimplantation Mouse Embryo1

Alarcón

2010

Biology of Reproduction

133

125

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In preimplantation mouse development, the first cell lineages to be established are the trophectoderm (TE) and inner cell mass. TE possesses epithelial features, including apical-basal cell polarity and intercellular junctions, which are crucial to generate a fluid-filled cavity in the blastocyst. Homologs of the partitioning defective (par) genes in Caenorhabditis elegans are critical regulators of cell polarity. However, their roles in regulating TE differentiation and blastocyst formation remain unclear. Here, the role of mouse Pard6b, a homolog of par-6 gene and a component of the PAR-atypical protein kinase C (aPKC) complex, was investigated. Pard6b expression was knocked down by microinjecting RNA interference construct into zygotes. Pard6b-knockdown embryos cleaved and compacted normally but failed to form the blastocyst cavity. The cavitation failure is likely the result of defective intercellular junctions, because Pard6b knockdown caused abnormal distribution of actin filaments and TJP1 (ZO-1) tight junction (TJ) protein and interfered with cavitation in chimeras containing cells from normal embryos. Defective TJ formation may be caused by abnormal cell polarization, because the apical localization of PRKCZ (aPKCzeta) was absent in Pard6b-knockdown embryos. Pard6b knockdown also diminished the expression of CDX2, a TE-lineage transcription factor, in the outer cells. TEAD4, a transcriptional activator that is required for Cdx2 expression and cavity formation, was not essential for the transcription of Pard6b. Taken together, Pard6b is necessary for blastocyst morphogenesis, particularly the development of TE-specific features-namely, the apical-basal cell polarity, formation of TJ, paracellular permeability sealing, and up-regulated expression of Cdx2.

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“…Depletion of ZO-2 protein by RNA interference in two-cell embryos delays blastocoel cavity formation with normal cell proliferation and morphogenesis. In contrast, ZO-1 knockdown, or combined ZO-1 and ZO-2 knockdown, produces a more severe inhibition of blastocoel formation, indicating distinct but possibly overlapping roles for ZO proteins in blastocyst morphogenesis (Sheth et al 2008). Further studies are needed to address these contradictions in ZO-2's role in cell proliferation, possibly because of different experimental systems/contexts, and to identify genes regulated by ZO-2 in association with SAF-B or other transcription factors.…”

Section: Zo-2 In Cell Proliferation and Gene Expressionmentioning

confidence: 97%

Junctional Music that the Nucleus Hears: Cell-Cell Contact Signaling and the Modulation of Gene Activity

McCrea

Gu²,

Balda³

2009

Cold Spring Harbor Perspectives in Biology

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Tight junction protein ZO-2 expression and relative function of ZO-1 and ZO-2 during mouse blastocyst formation

Cited by 40 publications

References 45 publications

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

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

Cell Polarity Regulator PARD6B Is Essential for Trophectoderm Formation in the Preimplantation Mouse Embryo1

Junctional Music that the Nucleus Hears: Cell-Cell Contact Signaling and the Modulation of Gene Activity

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