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ZIRC
ZFIN ID: ZDB-PUB-190117-8
Junction-based lamellipodia drive endothelial cell rearrangements in vivo via a VE-cadherin-F-actin based oscillatory cell-cell interaction
Paatero, I., Sauteur, L., Lee, M., Lagendijk, A.K., Heutschi, D., Wiesner, C., Guzmán, C., Bieli, D., Hogan, B.M., Affolter, M., Belting, H.G.
Date: 2018
Source: Nature communications   9: 3545 (Journal)
Registered Authors: Affolter, Markus, Belting, Heinz-Georg Paul (Henry), Hogan, Ben M., Paatero, Ilkka, Sauteur, Loïc
Keywords: none
MeSH Terms:
  • Actins/metabolism*
  • Animals
  • Animals, Genetically Modified
  • Antigens, CD/physiology*
  • Cadherins/physiology*
  • Cell Communication/physiology
  • Cell Movement/physiology*
  • Embryo, Nonmammalian
  • Endothelial Cells/physiology*
  • Intercellular Junctions/physiology
  • Pseudopodia/physiology*
  • Zebrafish Proteins/metabolism
  • Zonula Occludens-1 Protein/metabolism
PubMed: 30171187 Full text @ Nat. Commun.
FIGURES
ABSTRACT
Angiogenesis and vascular remodeling are driven by extensive endothelial cell movements. Here, we present in vivo evidence that endothelial cell movements are associated with oscillating lamellipodia-like structures, which emerge from cell junctions in the direction of cell movements. High-resolution time-lapse imaging of these junction-based lamellipodia (JBL) shows dynamic and distinct deployment of junctional proteins, such as F-actin, VE-cadherin and ZO1, during JBL oscillations. Upon initiation, F-actin and VE-cadherin are broadly distributed within JBL, whereas ZO1 remains at cell junctions. Subsequently, a new junction is formed at the front of the JBL, which then merges with the proximal junction. Rac1 inhibition interferes with JBL oscillations and disrupts cell elongation-similar to a truncation in ve-cadherin preventing VE-cad/F-actin interaction. Taken together, our observations suggest an oscillating ratchet-like mechanism, which is used by endothelial cells to move over each other and thus provides the physical means for cell rearrangements.
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