AmotL2 links VE-cadherin to contractile actin fibres necessary for aortic lumen expansion

Sara Hultin, Yujuan Zheng, Mahdi Mojallal, Simona Vertuani, Christian Gentili, Martial Balland, Rachel Milloud, Heinz-Georg Belting, Markus Affolter, Christian S.M. Helker, Ralf H. Adams, Wiebke Herzog, Per Uhlen, Arindam Majumdar and Lars Holmgren ()
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Sara Hultin: Cancer Center Karolinska, Karolinska University Hospital
Yujuan Zheng: Cancer Center Karolinska, Karolinska University Hospital
Mahdi Mojallal: Cancer Center Karolinska, Karolinska University Hospital
Simona Vertuani: Cancer Center Karolinska, Karolinska University Hospital
Christian Gentili: Cancer Center Karolinska, Karolinska University Hospital
Martial Balland: Laboratoire interdisciplinaire de Physique, Université Joseph Fourier (Grenoble 1), Domaine Universitaire, Bat. E45 140, rue de la physique, Saint Martin d´Hères Cedex 9 38402 Grenoble, France
Rachel Milloud: Laboratoire interdisciplinaire de Physique, Université Joseph Fourier (Grenoble 1), Domaine Universitaire, Bat. E45 140, rue de la physique, Saint Martin d´Hères Cedex 9 38402 Grenoble, France
Heinz-Georg Belting: Abt. Zellbiologie, Biozentrum/Uni Basel
Markus Affolter: Abt. Zellbiologie, Biozentrum/Uni Basel
Christian S.M. Helker: Biological Faculty, University of Muenster
Ralf H. Adams: Max Planck Institute for Molecular Biomedicine
Wiebke Herzog: Biological Faculty, University of Muenster
Per Uhlen: Karolinska Institute
Arindam Majumdar: Cancer Center Karolinska, Karolinska University Hospital
Lars Holmgren: Cancer Center Karolinska, Karolinska University Hospital

Nature Communications, 2014, vol. 5, issue 1, 1-13

Abstract: 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.

Date: 2014
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DOI: 10.1038/ncomms4743

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