PUBLICATION

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

Authors
Hultin, S., Zheng, Y., Mojallal, M., Vertuani, S., Gentili, C., Balland, M., Milloud, R., Belting, H.G., Affolter, M., Helker, C.S., Adams, R.H., Herzog, W., Uhlen, P., Majumdar, A., Holmgren, L.
ID
ZDB-PUB-140513-22
Date
2014
Source
Nature communications   5: 3743 (Journal)
Registered Authors
Affolter, Markus, Belting, Heinz-Georg Paul (Henry), Helker, Christian, Herzog, Wiebke, Holmgren, Lars, Majumdar, Arindam
Keywords
none
MeSH Terms
  • Actin Cytoskeleton/metabolism
  • Adherens Junctions/metabolism
  • Animals
  • Antigens, CD/metabolism*
  • Aorta/cytology
  • Aorta/growth & development*
  • Cadherins/metabolism*
  • Cell Communication
  • Cell Shape
  • Contractile Proteins/metabolism*
  • Endothelial Cells/cytology
  • Endothelium, Vascular/growth & development
  • Endothelium, Vascular/metabolism
  • Extracellular Matrix/metabolism
  • Gene Knockdown Techniques
  • Membrane Proteins/metabolism*
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Morphogenesis
  • Morpholinos/genetics
  • Neovascularization, Physiologic/physiology*
  • RNA Interference
  • RNA, Small Interfering
  • Zebrafish
  • Zebrafish Proteins/metabolism*
PubMed
24806444 Full text @ Nat. Commun.
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.
Genes / Markers
Figures
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Expression
Phenotype
Mutation and Transgenics
Human Disease / Model Data
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping
Errata and Notes