edoc

AmotL2 Links VE-cadherin to Contractile Actin Fibres Necessary for Aortic Lumen Expansion

Hultin, Sara and Zheng, Yujuan and Mojallal, Mahdi and Vertuani, Simona and Gentili, Christian and Balland, Martial and Milloud, Rachel and Belting, Heinz-Georg and Affolter, Markus and Helker, Christian S. M. and Adams, Ralf H. and Herzog, Wiebke and Uhlen, Per and Majumdar, Arindam and Holmgren, Lars. (2014) AmotL2 Links VE-cadherin to Contractile Actin Fibres Necessary for Aortic Lumen Expansion. Nature communications, Vol. 5 , Article Nr. 3743.

Full text not available from this repository.

Official URL: http://edoc.unibas.ch/dok/A6263121

Downloads: Statistics Overview

Abstract

The assembly of individual endothelial cells into multicellular tubes is a complex morphogenetic event in vascular development. Extracellular matrix cues and cell-cell junctional communication are fundamental to tube formation. Together they determine the shape of endothelial cells and the tubular structures that they ultimately form. Little is known regarding how mechanical signals are transmitted between cells to control cell shape changes during morphogenesis. Here we provide evidence that the scaffold protein amotL2 is needed for aortic vessel lumen expansion. Using gene inactivation strategies in zebrafish, mouse and endothelial cell culture systems, we show that amotL2 associates to the VE-cadherin adhesion complex where it couples adherens junctions to contractile actin fibres. Inactivation of amotL2 dissociates VE-cadherin from cytoskeletal tensile forces that affect endothelial cell shape. We propose that the VE-cadherin/amotL2 complex is responsible for transmitting mechanical force between endothelial cells for the coordination of cellular morphogenesis consistent with aortic lumen expansion and function.
Faculties and Departments:05 Faculty of Science > Departement Biozentrum > Growth & Development > Cell Biology (Affolter)
UniBasel Contributors:Affolter, Markus
Item Type:Article, refereed
Article Subtype:Research Article
Bibsysno:Link to catalogue
Publisher:Nature Publishing Group
ISSN:2041-1723
Note:Publication type according to Uni Basel Research Database: Journal article
Related URLs:
Identification Number:
Last Modified:20 Jun 2014 07:56
Deposited On:20 Jun 2014 07:56

Repository Staff Only: item control page