PUBLICATION

Control of dynamic cell behaviors during angiogenesis and anastomosis by Rasip1

Authors
Lee, M., Betz, C., Yin, J., Paatero, I., Schellinx, N., Carte, A.N., Wilson, C.W., Ye, W., Affolter, M., Belting, H.G.
ID
ZDB-PUB-210813-9
Date
2021
Source
Development (Cambridge, England)   148(15): (Journal)
Registered Authors
Affolter, Markus, Belting, Heinz-Georg Paul (Henry), Paatero, Ilkka
Keywords
Anastomosis, Angiogenesis, Endothelial cells, Rasip1, VE-cadherin, Zebrafish
MeSH Terms
  • Actin Cytoskeleton/metabolism
  • Actins/metabolism
  • Animals
  • Cell Communication/physiology
  • Endothelial Cells/metabolism
  • Endothelial Cells/physiology
  • Intercellular Junctions/metabolism
  • Intercellular Junctions/physiology
  • Intracellular Signaling Peptides and Proteins/metabolism*
  • Membrane Proteins/metabolism
  • Morphogenesis/physiology
  • Neovascularization, Physiologic/physiology*
  • Zebrafish/metabolism*
  • Zebrafish/physiology
  • Zebrafish Proteins/metabolism*
PubMed
34383884 Full text @ Development
Abstract
Organ morphogenesis is driven by a wealth of tightly orchestrated cellular behaviors, which ensure proper organ assembly and function. Many of these cell activities involve cell-cell interactions and remodeling of the F-actin cytoskeleton. Here, we analyze the requirement for Rasip1 (Ras-interacting protein 1), an endothelial-specific regulator of junctional dynamics, during blood vessel formation. Phenotype analysis of rasip1 mutants in zebrafish embryos reveals distinct functions of Rasip1 during sprouting angiogenesis, anastomosis and lumen formation. During angiogenic sprouting, loss of Rasip1 causes cell pairing defects due to a destabilization of tricellular junctions, indicating that stable tricellular junctions are essential to maintain multicellular organization within the sprout. During anastomosis, Rasip1 is required to establish a stable apical membrane compartment; rasip1 mutants display ectopic, reticulated junctions and the apical compartment is frequently collapsed. Loss of Ccm1 and Heg1 function mimics the junctional defects of rasip1 mutants. Furthermore, downregulation of ccm1 and heg1 leads to a delocalization of Rasip1 at cell junctions, indicating that junctional tethering of Rasip1 is required for its function in junction formation and stabilization during sprouting angiogenesis.
Genes / Markers
Figures
Show all Figures
Expression
Phenotype
Mutation and Transgenics
Human Disease / Model Data
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping
Errata and Notes