scholarly journals CADHERIN mediated AMIS localisation

2021 ◽  
Author(s):  
Xuan Liang ◽  
Antonia Weberling ◽  
Chun Yuan Hii ◽  
Magdalena Zernicka-Goetz ◽  
Clare E Buckley
Keyword(s):  
Cell Adhesion ◽  
Cell Division ◽  
De Novo ◽  
Embryonic Stem ◽  
Cellular Tissue ◽  
Initiation Site ◽  
Stage Of Development ◽  
Independent Mechanism ◽  
Epithelial Structure ◽  
Cell Cell

Individual cells within de novo polarising tubes and cavities must integrate their forming apical domains into a centralised apical membrane initiation site (AMIS). This is necessary to enable organised lumen formation within multi-cellular tissue. Despite the well documented importance of cell division in localising the AMIS, we have found a division-independent mechanism of AMIS localisation that relies instead on CADHERIN-mediated cell-cell adhesion. Our study of de novo polarising mouse embryonic stem cells (mESCs) cultured in 3D suggest that cell-cell adhesion directs the localisation of apical proteins such as PAR-6 to a centralised AMIS. Unexpectedly, we also found that mESC cell clusters lacking functional E-CADHERIN were still able to form a lumen-like cavity in the absence of AMIS localisation and did so at a later stage of development via a closure mechanism, instead of via hollowing. This work suggests that there are two, interrelated mechanisms of apical polarity localisation: cell adhesion and cell division. Alignment of these mechanisms in space allows for redundancy in the system and ensures the development of a coherent epithelial structure within a growing organ.

scholarly journals Maturation of Embryonic Stem Cells Into Endothelial Cells in an In Vitro Model of Vasculogenesis

Blood ◽  
1999 ◽  
Vol 93 (4) ◽  
pp. 1253-1263 ◽  
Author(s):  
Masanori Hirashima ◽  
Hiroshi Kataoka ◽  
Satomi Nishikawa ◽  
Norihisa Matsuyoshi ◽  
Shin-Ichi Nishikawa
Keyword(s):  
Cell Adhesion ◽  
Endothelial Cell ◽  
Growth Factor ◽  
Culture System ◽  
Molecular Mechanisms ◽  
Es Cells ◽  
Embryonic Stem ◽  
Vascular Endothelial ◽  
Cell Cell

A primitive vascular plexus is formed through coordinated regulation of differentiation, proliferation, migration, and cell-cell adhesion of endothelial cell (EC) progenitors. In this study, a culture system was devised to investigate the behavior of purified EC progenitors in vitro. Because Flk-1+ cells derived from ES cells did not initially express other EC markers, they were sorted and used as EC progenitors. Their in vitro differentiation into ECs, via vascular endothelial-cadherin (VE-cadherin)+ platelet-endothelial cell adhesion molecule-1 (PECAM-1)+ CD34−to VE-cadherin+ PECAM-1+CD34+ stage, occurred without exogenous factors, whereas their proliferation, particularly at low cell density, required OP9 feeder cells. On OP9 feeder layer, EC progenitors gave rise to sheet-like clusters of Flk-1+ cells, with VE-cadherin concentrated at the cell-cell junction. The growth was suppressed by Flt-1-IgG1 chimeric protein and dependent on vascular endothelial growth factor (VEGF) but not placenta growth factor (PIGF). Further addition of VEGF resulted in cell dispersion, indicating the role of VEGF in the migration of ECs as well as their proliferation. Cell-cell adhesion of ECs in this culture system was mediated by VE-cadherin. Thus, the culture system described here is useful in dissecting the cellular events of EC progenitors that occur during vasculogenesis and in investigating the molecular mechanisms underlying these processes.

Abstract 361: Creg1 Interacts With Sec8 to Promote Cell-cell Adhesion During Cardiomyogenesis

2016 ◽  
Vol 119 (suppl_1) ◽  
Author(s):  
Jie Liu ◽  
Yanmei Qi ◽  
Shu-Chan Hsu ◽  
Siavash Saadat ◽  
Saum Rahimi ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Es Cells ◽  
Embryonic Stem ◽  
Intercellular Junctions ◽  
Amino Acid Residues ◽  
Loss Of Function ◽  
Wild Type ◽  
Adhesion Sites ◽  
Cell Cell

Cellular repressor of E1A-stimulated genes 1 (CREG1) is a 24 kD glycoprotein essential for early embryonic development. Our immunofluorescence studies revealed that CREG1 is highly expressed at myocyte junctions in both embryonic and adult hearts. To explore it role in cardiomyogenesis, we employed gain- and loss-of-function analyses demonstrating that CREG1 is required for the differentiation of mouse embryonic stem (ES) cell into cohesive myocardium-like structures. Chimeric cultures of wild-type and CREG1 knockout ES cells expressing cardiac-specific reporters showed that the cardiomyogenic effect of CREG1 is cell autonomous. Furthermore, we identified a novel interaction between CREG1 and Sec8 of the exocyst complex, which tethers vesicles to the plasma membrane. Mutations of the amino acid residues D141 and P142 to alanine in CREG1 abolished its binding to Sec8. To address the role of the CREG1-Sec8 interaction in cardiomyogenesis, we rescued CREG1 knockout ES cells with wild-type and Sec8-binding mutant CREG1 and showed that CREG1 binding to Sec8 promotes cardiomyocyte differentiation and cohesion. Mechanistically, CREG1, Sec8 and N-cadherin all localize at cell-cell adhesion sites. CREG1 overexpression enhances the assembly of adherens and gap junctions. By contrast, its knockout inhibits the Sec8-N-cadherin interaction and induces their degradation. Finally, shRNA-mediated knockdown of Sec8 leads to cardiomyogenic defects similar to CREG1 knockout. These results suggest that the CREG1 binding to Sec8 enhances the assembly of intercellular junctions and promotes cardiomyogenesis.

scholarly journals Lipid Phosphate Phosphatase 3 Stabilization of β-Catenin Induces Endothelial Cell Migration and Formation of Branching Point Structures

2010 ◽  
Vol 30 (7) ◽  
pp. 1593-1606 ◽  
Author(s):  
Joseph O. Humtsoe ◽  
Mingyao Liu ◽  
Asrar B. Malik ◽  
Kishore K. Wary
Keyword(s):  
Cell Adhesion ◽  
Endothelial Cell ◽  
De Novo ◽  
Endothelial Cell Migration ◽  
Dependent Manner ◽  
P120 Catenin ◽  
Branching Point ◽  
Lipid Phosphate ◽  
Underlying Mechanisms ◽  
Cell Cell

ABSTRACT Endothelial cell (EC) migration, cell-cell adhesion, and the formation of branching point structures are considered hallmarks of angiogenesis; however, the underlying mechanisms of these processes are not well understood. Lipid phosphate phosphatase 3 (LPP3) is a recently described p120-catenin-associated integrin ligand localized in adherens junctions (AJs) of ECs. Here, we tested the hypothesis that LPP3 stimulates β-catenin/lymphoid enhancer binding factor 1 (β-catenin/LEF-1) to induce EC migration and formation of branching point structures. In subconfluent ECs, LPP3 induced expression of fibronectin via β-catenin/LEF-1 signaling in a phosphatase and tensin homologue (PTEN)-dependent manner. In confluent ECs, depletion of p120-catenin restored LPP3-mediated β-catenin/LEF-1 signaling. Depletion of LPP3 resulted in destabilization of β-catenin, which in turn reduced fibronectin synthesis and deposition, which resulted in inhibition of EC migration. Accordingly, reexpression of β-catenin but not p120-catenin in LPP3-depleted ECs restored de novo synthesis of fibronectin, which mediated EC migration and formation of branching point structures. In confluent ECs, however, a fraction of p120-catenin associated and colocalized with LPP3 at the plasma membrane, via the C-terminal cytoplasmic domain, thereby limiting the ability of LPP3 to stimulate β-catenin/LEF-1 signaling. Thus, our study identified a key role for LPP3 in orchestrating PTEN-mediated β-catenin/LEF-1 signaling in EC migration, cell-cell adhesion, and formation of branching point structures.

scholarly journals Rapid Suppression of Activated Rac1 by Cadherins and Nectins during De Novo Cell-Cell Adhesion

PLoS ONE ◽  
2011 ◽  
Vol 6 (3) ◽  
pp. e17841 ◽  
Author(s):  
Khameeka N. Kitt ◽  
W. James Nelson
Keyword(s):  
Cell Adhesion ◽  
De Novo ◽  
Cell Cell

A Study of a Mechanism of Cell Proliferation Promotion of Cultured Osteoblasts by Mechanical Vibration

2018 ◽  
Author(s):  
Toshihiko Shiraishi ◽  
Akitoshi Nishijima
Keyword(s):  
Cell Proliferation ◽  
Cell Adhesion ◽  
Cell Division ◽  
Western Blot ◽  
Mechanical Vibration ◽  
Nuclear Fraction ◽  
Analysis Software ◽  
Pile Up ◽  
Western Blot Experiment ◽  
Cell Cell

This paper describes a mechanism of cell proliferation promotion of cultured osteoblasts by mechanical vibration focusing on β-catenin. 12.5 Hz and 0.5 G mechanical vibration was reported to promote the cell proliferation of cultured osteoblasts in plane culture. That is because the mechanical vibration weakens cell-cell adhesion, promotes to pile up cells, and allows cells to form multilayer structure. However, it has not been clarified why cells continue cell division after their monolayer confluent state. Here we show that mechanical vibration not only weakens cell-cell adhesion bound by β-catenin but also promotes to move β-catenin from the cytoplasm to the nuclei, where β-catenin associates with DNA-binding members of the Tcf/LEF family and other associated transcription factors including cell division. After osteoblastic cells were cultured under 12.5 Hz and 0.5 G mechanical vibration, cells were fractionated into nuclear and cytoplasmic fractions using a centrifugation method. β-catenin in each fraction was detected by a western blot experiment. The protein bands from western blot films were quantified with an image processing and analysis software, ImageJ. As a result, the vibration group gave higher expression of β-catenin in nuclear fraction than the non-vibration group just after the vibration group reached the saturated cell density. It indicates that 12.5 Hz and 0.5 G mechanical vibration may promote to move β-catenin into the nuclei and the cell division.

scholarly journals Computational modelling of epidermal stratification highlights the importance of asymmetric cell division for predictable and robust layer formation

2014 ◽  
Vol 11 (99) ◽  
pp. 20140631 ◽  
Author(s):  
Alexander Gord ◽  
William R. Holmes ◽  
Xing Dai ◽  
Qing Nie
Keyword(s):  
Cell Adhesion ◽  
Cell Division ◽  
Asymmetric Cell Division ◽  
Three Dimensional ◽  
Interaction Strength ◽  
Computational Modelling ◽  
Protective Layer ◽  
The Body ◽  
Cell Interactions ◽  
Cell Cell

Skin is a complex organ tasked with, among other functions, protecting the body from the outside world. Its outermost protective layer, the epidermis, is comprised of multiple cell layers that are derived from a single-layered ectoderm during development. Using a new stochastic, multi-scale computational modelling framework, the anisotropic subcellular element method, we investigate the role of cell morphology and biophysical cell–cell interactions in the formation of this layered structure. This three-dimensional framework describes interactions between collections of hundreds to thousands of cells and (i) accounts for intracellular structure and morphology, (ii) easily incorporates complex cell–cell interactions and (iii) can be efficiently implemented on parallel architectures. We use this approach to construct a model of the developing epidermis that accounts for the internal polarity of ectodermal cells and their columnar morphology. Using this model, we show that cell detachment, which has been previously suggested to have a role in this process, leads to unpredictable, randomized stratification and that this cannot be abrogated by adjustment of cell–cell adhesion interaction strength. Polarized distribution of cell adhesion proteins, motivated by epithelial polarization, can however eliminate this detachment, and in conjunction with asymmetric cell division lead to robust and predictable development.

Cell-to-Cell Connection in Plant Grafting – Molecular Insights into Symplasmic Reconstruction

2021 ◽  
Author(s):  
Ken-ichi Kurotani ◽  
Michitaka Notaguchi
Keyword(s):  
Cell Adhesion ◽  
Time Course ◽  
De Novo ◽  
Molecular Transport ◽  
Wound Response ◽  
Future Research ◽  
Sequencing Data ◽  
Graft Interface ◽  
Vascular Formation ◽  
Cell Cell

Abstract Grafting is a means to connect tissues from two individual plants and grow a single chimeric plant through establishment of both apoplasmic and symplasmic connections. Recent molecular studies using RNA-sequencing data have provided genetic information on the processes involved in tissue reunion, including wound response, cell division, cell-cell adhesion, cell differentiation, and vascular formation. Thus, studies on grafting increase our understanding of various aspects of plant biology. Grafting has also been used to study systemic signaling and transport of micro- and macromolecules in the plant body. Given that graft viability and molecular transport across graft junctions largely depend on vascular formation, a major focus in grafting biology has been the mechanism of vascular development. In addition, it has been thought that symplasmic connections via plasmodesmata are fundamentally important to share cellular information among newly proliferated cells at the graft interface and to accomplish tissue differentiation correctly. Therefore, this review focuses on plasmodesmata formation during grafting. We take advantage of interfamily grafts for unambiguous identification of the graft interface and summarize morphological aspects of de novo formation of plasmodesmata. Important molecular events are addressed by re-examining the time-course transcriptome of interfamily grafts, from which we recently identified the cell-cell adhesion mechanism. Plasmodesmata-associated genes upregulated during graft healing that may provide a link to symplasm establishment are described. We also discuss future research directions.

scholarly journals Regulation of cell–cell adhesion by the cadherin–catenin complex

2008 ◽  
Vol 36 (2) ◽  
pp. 149-155 ◽  
Author(s):  
W. James Nelson
Keyword(s):  
Cell Adhesion ◽  
Actin Cytoskeleton ◽  
Rho Gtpases ◽  
De Novo ◽  
Cytoplasmic Proteins ◽  
Cytoskeleton Reorganization ◽  
Dependent Cell ◽  
And Function ◽  
Cell Cell

Ca2+-dependent cell–cell adhesion is regulated by the cadherin family of cell adhesion proteins. Cadherins form trans-interactions on opposing cell surfaces which result in weak cell–cell adhesion. Stronger cell–cell adhesion occurs by clustering of cadherins and through changes in the organization of the actin cytoskeleton. Although cadherins were thought to bind directly to the actin cytoskeleton through cytoplasmic proteins, termed α- and β-catenin, recent studies with purified proteins indicate that the interaction is not direct, and instead an allosteric switch in α-catenin may mediate actin cytoskeleton reorganization. Organization and function of the cadherin–catenin complex are additionally regulated by phosphorylation and endocytosis. Direct studies of cell–cell adhesion has revealed that the cadherin–catenin complex and the underlying actin cytoskeleton undergo a series of reorganizations that are controlled by the Rho GTPases, Rac1 and RhoA, that result in the expansion and completion of cell–cell adhesion. In the present article, in vitro protein assembly studies and live-cell studies of de novo cell–cell adhesion are discussed in the context of how the cadherin–catenin complex and the actin cytoskeleton regulate cell–cell adhesion.

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