The role of apical cell-cell junctions and associated cytoskeleton in mechanotransduction

2017 ◽  
Vol 109 (4) ◽  
pp. 139-161 ◽  
Author(s):  
Sophie Sluysmans ◽  
Ekaterina Vasileva ◽  
Domenica Spadaro ◽  
Jimit Shah ◽  
Florian Rouaud ◽  
...  
Keyword(s):  
Apical Cell ◽  
Cell Junctions ◽  
Cell Cell

Increased levels of the Drosophila Abelson tyrosine kinase in nerves and muscles: subcellular localization and mutant phenotypes imply a role in cell-cell interactions

Development ◽  
1992 ◽  
Vol 116 (4) ◽  
pp. 953-966 ◽  
Author(s):  
R.L. Bennett ◽  
F.M. Hoffmann
Keyword(s):  
Nervous System ◽  
Tyrosine Kinase ◽  
Expression Patterns ◽  
Apical Cell ◽  
Cell Interactions ◽  
Cell Junctions ◽  
Imaginal Disk ◽  
Abelson Tyrosine Kinase ◽  
Mutant Phenotypes ◽  
Cell Cell

Mutations in the Drosophila Abelson tyrosine kinase have pleiotropic effects late in development that lead to pupal lethality or adults with a reduced life span, reduced fecundity and rough eyes. We have examined the expression of the abl protein throughout embryonic and pupal development and analyzed mutant phenotypes in some of the tissues expressing abl. abl protein, present in all cells of the early embryo as the product of maternally contributed mRNA, transiently localizes to the region below the plasma membrane cleavage furrows as cellularization initiates. The function of this expression is not yet known. Zygotic expression of abl is first detected in the post-mitotic cells of the developing muscles and nervous system midway through embryogenesis. In later larval and pupal stages, abl protein levels are also highest in differentiating muscle and neural tissue including the photoreceptor cells of the eye. abl protein is localized subcellularly to the axons of the central nervous system, the embryonic somatic muscle attachment sites and the apical cell junctions of the imaginal disk epithelium. Evidence for abl function was obtained by analysis of mutant phenotypes in the embryonic somatic muscles and the eye imaginal disk. The expression patterns and mutant phenotypes indicate a role for abl in establishing and maintaining cell-cell interactions.

scholarly journals Claudin Family of Proteins and Cancer: An Overview

2010 ◽  
Vol 2010 ◽  
pp. 1-11 ◽  
Author(s):  
Amar B. Singh ◽  
Ashok Sharma ◽  
Punita Dhawan
Keyword(s):  
Cell Adhesion ◽  
Tight Junction ◽  
Tight Junctions ◽  
Apical Cell ◽  
Cellular Transformation ◽  
Molecular Architecture ◽  
Human Carcinoma ◽  
Potential Implication ◽  
Cell Cell

Tight junctions are the apical cell-cell adhesion that regulate paracellular permeability and are critical for epithelial cell polarity. Molecular architecture of tight junction has been studied extensively, which has confirmed that claudin family of proteins is integral component of tight junction. Loss of cell-cell adhesion is central to the cellular transformation and acquisition of metastatic potential; however, the role of claudin family of proteins play in a series of pathophysiological events, including human carcinoma development, is only now beginning to be understood. Several claudin mouse knockout models have been generated and the diversity of phenotypes observed clearly demonstrates their important roles in the maintenance of tissue integrity in various organs and suggest that claudins also participate in cellular contexts other than tight junctions. The mechanisms of claudin regulation and their exact roles in normal physiology and disease are being elucidated, but much work remains to be done. In this review, we have discussed the conceptual framework concerning claudins and their potential implication in cancer. We predict that next several years will likely witness a boom in our understanding of the potential role of claudins in the regulation of tumorigenesis, which may, in turn, provide new approaches for the targeted therapy.

ROLE OF CELL-CELL JUNCTIONS IN MEDIATING ENDOTHELIAL CELL RESPONSES TO FLUID SHEAR STRESS

2004 ◽  
Vol 13 (3) ◽  
pp. 41
Author(s):  
Eleni Tzima ◽  
Mohamed Irani-Tehrani ◽  
Elizabetta Dejana ◽  
Martin Schwartz
Keyword(s):  
Shear Stress ◽  
Endothelial Cell ◽  
Fluid Shear Stress ◽  
Cell Junctions ◽  
Fluid Shear ◽  
Cell Responses ◽  
Cell Cell

scholarly journals Heat Shock Protein 27 Associates with Basolateral Cell Boundaries in Heat-Shocked and ATP-Depleted Epithelial Cells

2002 ◽  
Vol 13 (2) ◽  
pp. 332-341
Author(s):  
Eric A. Shelden ◽  
Michael J. Borrelli ◽  
Fiona M. Pollock ◽  
Rita Bonham
Keyword(s):  
Heat Stress ◽  
Heat Shock ◽  
Epithelial Cells ◽  
Apical Cell ◽  
Atp Depletion ◽  
Cell Junctions ◽  
Cell Contact ◽  
Double Labeling ◽  
Cell Substrate ◽  
Cell Cell

ABSTRACT. Heat stress alters epithelial barrier function, and heat stress preconditioning protects epithelial function from injury. Hsp27 is a small stress protein that has previously been shown to modulate actin assembly. Thus, by regulating actin filaments associated with cell junctions, hsp27 could alter epithelial function. To begin to address this hypothesis, the regulation and distribution of a human hsp27-green fluorescence fusion protein (EGFPhHsp27) that is expressed in cultured renal epithelial cells was assessed. EGFPhHsp27, like the endogenous hsp27, associated with the cytoskeleton in heat-stressed and chemically ATP-depleted cells, and both proteins were regulated similarly. Confocal microscopy of intact and detergent-lysed cells revealed novel distribution patterns in which EGFPhHsp27 associated with basolateral, but not apical, cell borders in injured cells. Double labeling studies revealed EGFPhHsp27 and actin filament colocalization in ATP-depleted cells. However, during heat shock, granules of EGFPhHsp27 were found at sites of cell-cell contact and in the cell body, but colocalization with actin was not apparent. Thus, heat stress and ATP depletion induce distinct patterns of hsp27 redistribution in epithelial cells, and sites of cell-cell and cell-substrate attachment are unique in their ability to recruit hsp27 during injury. The association of EGFPhHsp27 with basolateral cell boundaries supports a potential role for hsp27 in protection or regulation of epithelial cell-cell and cell-substrate attachments.

scholarly journals Myosin IIA–mediated forces regulate multicellular integrity during vascular sprouting

2019 ◽  
Vol 30 (16) ◽  
pp. 1974-1984 ◽  
Author(s):  
Christine Yoon ◽  
Colin Choi ◽  
Sarah Stapleton ◽  
Teodelinda Mirabella ◽  
Caroline Howes ◽  
...  
Keyword(s):  
Network Formation ◽  
Critical Role ◽  
Three Dimensional ◽  
Adherens Junction ◽  
Cell Junctions ◽  
Cell Contractility ◽  
Surrounding Matrix ◽  
Contractile Forces ◽  
Cell Cell

Angiogenic sprouting is a critical process involved in vascular network formation within tissues. During sprouting, tip cells and ensuing stalk cells migrate collectively into the extracellular matrix while preserving cell–cell junctions, forming patent structures that support blood flow. Although several signaling pathways have been identified as controlling sprouting, it remains unclear to what extent this process is mechanoregulated. To address this question, we investigated the role of cellular contractility in sprout morphogenesis, using a biomimetic model of angiogenesis. Three-dimensional maps of mechanical deformations generated by sprouts revealed that mainly leader cells, not stalk cells, exert contractile forces on the surrounding matrix. Surprisingly, inhibiting cellular contractility with blebbistatin did not affect the extent of cellular invasion but resulted in cell–cell dissociation primarily between tip and stalk cells. Closer examination of cell–cell junctions revealed that blebbistatin impaired adherens-junction organization, particularly between tip and stalk cells. Using CRISPR/Cas9-mediated gene editing, we further identified NMIIA as the major isoform responsible for regulating multicellularity and cell contractility during sprouting. Together, these studies reveal a critical role for NMIIA-mediated contractile forces in maintaining multicellularity during sprouting and highlight the central role of forces in regulating cell–cell adhesions during collective motility.

Cytokinesis and the establishment of early embryonic cell polarity

2008 ◽  
Vol 36 (3) ◽  
pp. 384-386 ◽  
Author(s):  
David R. Burgess
Keyword(s):  
Epithelial Cells ◽  
Cell Polarity ◽  
Primary Cilia ◽  
Embryonic Cell ◽  
Cell Junctions ◽  
Cell Contact ◽  
Apical Surface ◽  
Integral Role ◽  
Cell Cell

Cleavage divisions in many animals form a blastula made up of a simple polarized epithelium. This simple embryonic epithelium possesses an apical surface covered with microvilli and primary cilia separated from the basolateral surfaces by cell–cell junctions. The apical membrane proteins and lipids differ from those of the basolateral on these embryonic epithelial cells, as is found in adult epithelial cells. Formation of cell polarity in embryos at fertilization, including those from both protostomes and deuterostomes, uses the same molecules and signalling machinery as do polarizing epithelial cells that polarize upon cell–cell contact. In addition, the actin–myosin cytoskeleton plays an integral role in establishment and maintenance of this early cell polarity. However, early cleaving blastomeres from higher organisms including echinoderms and vertebrates have not been considered to exhibit cell polarity until formation of junctions at the third through to the fifth cleavage divisions. The role of new membrane addition into the late cleavage furrow during the early rounds of cytokinesis may play a key role in the early establishment of cell polarity in all animal embryos.

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