The single<i>Drosophila</i>ZO-1 protein Polychaetoid regulates embryonic morphogenesis in coordination with Canoe/afadin and Enabled

Choi, Wangsun; Jung, Kuo Chen; Nelson, Kevin S.; Bhat, Manzoor A.; Beitel, Greg J.; Peifer, Mark; Fanning, Alan S.

doi:10.1091/mbc.e10-12-1014

Cited by 63 publications

(83 citation statements)

References 69 publications

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“…Although Rap1 has been shown to regulate N-cadherin-based AJs and polarity in neuronal cells (Jossin and Cooper, 2011), the upregulation of N-cadherin in the lens epithelium of Rap1 cKO mice could be a secondary response to the altered epithelial plasticity and EMT noted in these lenses since elevated levels of collagen in cells undergoing EMT have been shown to upregulate N-cadherin (Shintani et al, 2008). The loss of ZO-1 based cell adhesive interactions observed in Rap1 deficient lenses in this study support earlier observations reported in cultured epithelial cells and in Drosophila lacking Rap1 and its effector molecule afadin (Choi et al, 2011; Mandai et al, 2013; Mandell et al, 2005; Ooshio et al, 2010; Pannekoek et al, 2009). These changes could be also arising in part from impaired formation of AJs, because conditional deletion of E-cadherin has been shown to impair formation of ZO-1-based cell-cell junctions in the mouse lens epithelium (Pontoriero et al, 2009).…”

Section: Discussionsupporting

confidence: 92%

Rap1 GTPase is required for mouse lens epithelial maintenance and morphogenesis

Maddala

Nagendran

Lang

et al. 2015

Developmental Biology

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Rap1, a Ras-like small GTPase, plays a crucial role in cell-matrix adhesive interactions, cell-cell junction formation, cell polarity and migration. The role of Rap1 in vertebrate organ development and tissue architecture, however, remains elusive. We addressed this question in a mouse lens model system using a conditional gene targeting approach. While individual germline deficiency of either Rap1a or Rap1b did not cause overt defects in mouse lens, conditional double deficiency (Rap1 cKO) prior to lens placode formation led to an ocular phenotype including microphthalmia and lens opacification in embryonic mice. The embryonic Rap1 cKO mouse lens exhibited striking defects including loss of E-cadherin- and ZO-1-based cell-cell junctions, disruption of paxillin and β1-integrin-based cell adhesive interactions along with abnormalities in cell shape and apical-basal polarity of epithelium. These epithelial changes were accompanied by increased levels of α-smooth muscle actin, vimentin and N-cadherin, and expression of transcriptional suppressors of E-cadherin (Snai1, Slug and Zeb2), and a mesenchymal metabolic protein (Dihydropyrimidine dehydrogenase). Additionally, while lens differentiation was not overtly affected, increased apoptosis and dysregulated cell cycle progression were noted in epithelium and fibers in Rap1 cKO mice. Collectively these observations uncover a requirement for Rap1 in maintenance of lens epithelial phenotype and morphogenesis.

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Section: Discussionsupporting

confidence: 92%

Rap1 GTPase is required for mouse lens epithelial maintenance and morphogenesis

Maddala

Nagendran

Lang

et al. 2015

Developmental Biology

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“…We propose that cingulin, ZO-1, paracingulin, and PLEKHA7, together with afadin and other regulatory and cytoskeletal proteins, [50][51][52] are part of a molecular framework that links TJ to AJ (Fig. 1), and thus the apical to the lateral domain of polar-ized epithelial cells, by orchestrating the formation of a continuous circumferential belt at the apical junctional complex.…”

Section: Resultsmentioning

confidence: 99%

Cingulin, paracingulin, and PLEKHA7: signaling and cytoskeletal adaptors at the apical junctional complex

Citi

Pulimeno

Paschoud

2012

Annals of the New York Academy of Sciences

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Cingulin, paracingulin, and PLEKHA7 are proteins localized in the cytoplasmic region of the apical junctional complex of vertebrate epithelial cells. Cingulin has been detected at tight junctions (TJs), whereas paracingulin has been detected at both TJs and adherens junctions (AJs) and PLEKHA7 has been detected at AJs. One function of cingulin and paracingulin is to regulate the activity of Rho family GTPases at junctions through their direct interaction with guanidine exchange factors of RhoA and Rac1. Cingulin also contributes to the regulation of transcription of several genes in different types of cultured cells, in part through its ability to modulate RhoA activity. PLEKHA7, together with paracingulin, is part of a protein complex that links E-cadherin to the microtubule cytoskeleton at AJs. In this paper, we review the current knowledge about these proteins, including their discovery, the characterization of their expression, localization, structure, molecular interactions, and their roles in different developmental and disease model systems.

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“…The Drosophila Afadin ortholog, Canoe, is critical for linking the actin cytoskeleton to the AJ during the mechanical stresses of development (Choi et al, 2011; Sawyer et al, 2011). Additionally, Afadin appears to play a role in regulating actomyosin-mediated paracellular permeability through its interactions with the TJ transmembrane protein JAM-A, ZO-2 and PDZ-GEF1; this complex regulates apical actomyosin contraction via the small GTPases Rap2 and RhoA (Monteiro et al, 2013).…”

Section: Scaffold Proteins Regulate Rho Gtpase Output At Cell-cell Jumentioning

confidence: 99%

Rho GTPases and actomyosin: Partners in regulating epithelial cell-cell junction structure and function

Arnold

Stephenson

Miller

2017

Experimental Cell Research

124

118

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Epithelial tissues are defined by polarized epithelial cells that are integrated into tissues and exhibit barrier function in order to regulate what is allowed to pass between cells. Cell-cell junctions must be stable enough to promote barrier function and tissue integrity, yet plastic enough to remodel when necessary. This remarkable ability to dynamically sense and respond to changes in cell shape and tissue tension allows cell-cell junctions to remain functional during events that disrupt epithelial homeostasis including morphogenesis, wound healing, and cell division. In order to achieve this plasticity, both tight junctions and adherens junctions are coupled to the underlying actomyosin cytoskeleton. Here, we discuss the importance of the junctional linkage to actomyosin and how a localized zone of active RhoA along with other Rho GTPases work together to orchestrate junctional actomyosin dynamics. We focus on how scaffold proteins help coordinate Rho GTPases, their upstream regulators, and their downstream effectors for efficient, localized Rho GTPase signaling output. Additionally, we highlight important roles junctional actin-binding proteins play in addition to their traditional roles in organizing actin. Together, Rho GTPases, their regulators, and effectors form compartmentalized signaling modules that regulate actomyosin structure and contractility to achieve proper cell-cell adhesion and tissue barriers.

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The singleDrosophilaZO-1 protein Polychaetoid regulates embryonic morphogenesis in coordination with Canoe/afadin and Enabled

Cited by 63 publications

References 69 publications

Rap1 GTPase is required for mouse lens epithelial maintenance and morphogenesis

Rap1 GTPase is required for mouse lens epithelial maintenance and morphogenesis

Cingulin, paracingulin, and PLEKHA7: signaling and cytoskeletal adaptors at the apical junctional complex

Rho GTPases and actomyosin: Partners in regulating epithelial cell-cell junction structure and function

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