scholarly journals Asymmetric distribution of Echinoid defines the epidermal leading edge during Drosophila dorsal closure

2011 ◽  
Vol 192 (2) ◽  
pp. 335-348 ◽  
Author(s):  
Caroline Laplante ◽  
Laura A. Nilson
Keyword(s):  
Drosophila Melanogaster ◽  
Cell Adhesion ◽  
Actin Cytoskeleton ◽  
Adhesion Molecule ◽  
Cell Adhesion Molecule ◽  
Leading Edge ◽  
Scaffolding Protein ◽  
Asymmetric Distribution ◽  
Dorsal Closure ◽  
Dorsal Midline

During Drosophila melanogaster dorsal closure, lateral sheets of embryonic epidermis assemble an actomyosin cable at their leading edge and migrate dorsally over the amnioserosa, converging at the dorsal midline. We show that disappearance of the homophilic cell adhesion molecule Echinoid (Ed) from the amnioserosa just before dorsal closure eliminates homophilic interactions with the adjacent dorsal-most epidermal (DME) cells, which comprise the leading edge. The resulting planar polarized distribution of Ed in the DME cells is essential for the localized accumulation of actin regulators and for actomyosin cable formation at the leading edge and for the polarized localization of the scaffolding protein Bazooka/PAR-3. DME cells with uniform Ed fail to assemble a cable and protrude dorsally, suggesting that the cable restricts dorsal migration. The planar polarized distribution of Ed in the DME cells thus provides a spatial cue that polarizes the DME cell actin cytoskeleton, defining the epidermal leading edge and establishing its contractile properties.

Vascular-endothelial-cadherin modulates endothelial monolayer permeability

1999 ◽  
Vol 112 (12) ◽  
pp. 1915-1923 ◽  
Author(s):  
P.L. Hordijk ◽  
E. Anthony ◽  
F.P. Mul ◽  
R. Rientsma ◽  
L.C. Oomen ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Actin Cytoskeleton ◽  
Adhesion Molecule ◽  
Cell Adhesion Molecule ◽  
Transendothelial Migration ◽  
Stress Fibers ◽  
Vascular Endothelial ◽  
Monolayer Permeability ◽  
Actin Stress Fibers ◽  
Cell Cell

Vascular endothelial (VE)-cadherin is the endothelium-specific member of the cadherin family of homotypic cell adhesion molecules. VE-cadherin, but not the cell adhesion molecule platelet/endothelial cell adhesion molecule (PECAM-1), markedly colocalizes with actin stress fibers at cell-cell junctions between human umbilical vein endothelial cells. Inhibition of VE-cadherin-mediated, but not PECAM-1-mediated, adhesion induced reorganization of the actin cytoskeleton, loss of junctional VE-cadherin staining and loss of cell-cell adhesion. In functional assays, inhibition of VE-cadherin caused increased monolayer permeability and enhanced neutrophil transendothelial migration. In a complementary set of experiments, modulation of the actin cytoskeleton was found to strongly affect VE-cadherin distribution. Brief stimulation of the beta2-adrenergic receptor with isoproterenol induced a loss of actin stress fibers resulting in a linear, rather than ‘jagged’, VE-cadherin distribution. The concomitant, isoproterenol-induced, reduction in monolayer permeability was alleviated by a VE-cadherin-blocking antibody. Finally, cytoskeletal reorganization resulting from the inactivation of p21Rho caused a diffuse localization of VE-cadherin, which was accompanied by reduced cell-cell adhesion. Together, these data show that monolayer permeability and neutrophil transendothelial migration are modulated by VE-cadherin-mediated cell-cell adhesion, which is in turn controlled by the dynamics of the actin cytoskeleton.

scholarly journals Syntenin-1 and Ezrin Proteins Link Activated Leukocyte Cell Adhesion Molecule to the Actin Cytoskeleton

2014 ◽  
Vol 289 (19) ◽  
pp. 13445-13460 ◽  
Author(s):  
Cicerone Tudor ◽  
Joost te Riet ◽  
Christina Eich ◽  
Rolf Harkes ◽  
Nick Smisdom ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Actin Cytoskeleton ◽  
Adhesion Molecule ◽  
Cell Adhesion Molecule

The Drosophila melanogaster l(2)gl gene encodes a protein homologous to the cadherin cell-adhesion molecule family

1989 ◽  
Vol 133 (2) ◽  
pp. 425-436 ◽  
Author(s):  
Christian Klämbt ◽  
Stephan Müller ◽  
Reinhard Lützelschwab ◽  
Rita Rossa ◽  
Frank Totzke ◽  
...  
Keyword(s):  
Drosophila Melanogaster ◽  
Cell Adhesion ◽  
Adhesion Molecule ◽  
Cell Adhesion Molecule

scholarly journals Dynamic Regulation of Activated Leukocyte Cell Adhesion Molecule–mediated Homotypic Cell Adhesion through the Actin Cytoskeleton

2000 ◽  
Vol 11 (6) ◽  
pp. 2057-2068 ◽  
Author(s):  
Judith M. D. T. Nelissen ◽  
Inge M. Peters ◽  
Bart G. de Grooth ◽  
Yvette van Kooyk ◽  
Carl G. Figdor
Keyword(s):  
Cell Adhesion ◽  
Actin Cytoskeleton ◽  
Adhesion Molecule ◽  
Actin Polymerization ◽  
Cell Adhesion Molecule ◽  
Cluster Formation ◽  
Single Particle Tracking ◽  
Lateral Mobility ◽  
Surface Distribution ◽  
Dynamic Regulation

Restricted expression of activated leukocyte cell adhesion molecule (ALCAM) by hematopoietic cells suggests an important role in the immune system and hematopoiesis. To get insight into the mechanisms that control ALCAM-mediated adhesion we have investigated homotypic ALCAM–ALCAM interactions. Here, we demonstrate that the cytoskeleton regulates ALCAM-mediated cell adhesion because inhibition of actin polymerization by cytochalasin D (CytD) strongly induces homotypic ALCAM–ALCAM interactions. This induction of cell adhesion is likely due to clustering of ALCAM at the cell surface, which is observed after CytD treatment. Single-particle tracking demonstrated that the lateral mobility of ALCAM in the cell membrane is increased 30-fold after CytD treatment. In contrast, both surface distribution and adhesion of a glycosylphosphatidylinositol (GPI)-anchored ALCAM mutant are insensitive to CytD, despite the increase in lateral mobility of GPI-ALCAM upon CytD treatment. This demonstrates that clustering of ALCAM is essential for cell adhesion, whereas enhanced diffusion of ALCAM alone is not sufficient for cluster formation. In addition, upon ligand binding, both free diffusion and the freely dragged distance of wild-type ALCAM, but not of GPI-ALCAM, are reduced over time, suggesting strengthening of the cytoskeleton linkage. From these findings we conclude that activation of ALCAM-mediated adhesion is dynamically regulated through actin cytoskeleton-dependent clustering.

scholarly journals Cell height: Tao rising

2012 ◽  
Vol 199 (7) ◽  
pp. 1023-1024 ◽  
Author(s):  
Liang Cai ◽  
Keith E. Mostov
Keyword(s):  
Drosophila Melanogaster ◽  
Cell Adhesion ◽  
Squamous Cell ◽  
Adhesion Molecule ◽  
Lateral Surface ◽  
Cell Shape ◽  
Cell Adhesion Molecule ◽  
Follicular Epithelium ◽  
Shape Transition ◽  
Cell Height

During oogenesis in Drosophila melanogaster, the cells in the follicular epithelium of the ovary undergo a transition from a cuboidal to a squamous shape. In this issue, Gomez et al. (2012. J. Cell Biol. http://dx.doi.org/10.1083/jcb.201207150) show that the kinase Tao promotes the endocytosis of the cell adhesion molecule Fasciclin 2 from the lateral surface of the cell and is critical for the cuboidal to squamous cell shape transition. Their results indicate that Tao is rising as a regulator of cell height.

622: Von Hippel-Lindau Inactivation Downregulates the Cell-Cell Adhesion Molecule E Cadherin in Renal Cancer Cells

2005 ◽  
Vol 173 (4S) ◽  
pp. 170-170
Author(s):  
Maxine G. Tran ◽  
Miguel A. Esteban ◽  
Peter D. Hill ◽  
Ashish Chandra ◽  
Tim S. O'Brien ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Cancer Cells ◽  
Renal Cancer ◽  
Adhesion Molecule ◽  
Cell Adhesion Molecule ◽  
Von Hippel Lindau ◽  
E Cadherin ◽  
Cell Cell
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