PUBLICATION
Cdh5/VE-cadherin Promotes Endothelial Cell Interface Elongation via Cortical Actin Polymerization during Angiogenic Sprouting
- Authors
- Sauteur, L., Krudewig, A., Herwig, L., Ehrenfeuchter, N., Lenard, A., Affolter, M., Belting, H.G.
- ID
- ZDB-PUB-141107-3
- Date
- 2014
- Source
- Cell Reports 9: 504-13 (Journal)
- Registered Authors
- Affolter, Markus, Belting, Heinz-Georg Paul (Henry), Lenard, Anna
- Keywords
- none
- MeSH Terms
-
- Actin Cytoskeleton/metabolism
- Actins/metabolism*
- Animals
- Antigens, CD/genetics
- Antigens, CD/metabolism*
- Cadherins/genetics
- Cadherins/metabolism*
- Cell Movement
- Endothelial Cells/cytology
- Endothelial Cells/metabolism*
- Endothelial Cells/physiology
- Endothelium, Vascular/embryology
- Endothelium, Vascular/metabolism
- Intercellular Junctions/metabolism
- Myosins/metabolism
- Neovascularization, Physiologic*
- Polymerization
- Zebrafish/embryology
- Zebrafish/genetics
- Zebrafish/metabolism*
- PubMed
- 25373898 Full text @ Cell Rep.
Citation
Sauteur, L., Krudewig, A., Herwig, L., Ehrenfeuchter, N., Lenard, A., Affolter, M., Belting, H.G. (2014) Cdh5/VE-cadherin Promotes Endothelial Cell Interface Elongation via Cortical Actin Polymerization during Angiogenic Sprouting. Cell Reports. 9:504-13.
Abstract
Organ morphogenesis requires the coordination of cell behaviors. Here, we have analyzed dynamic endothelial cell behaviors underlying sprouting angiogenesis in vivo. Two different mechanisms contribute to sprout outgrowth: tip cells show strong migratory behavior, whereas extension of the stalk is dependent upon cell elongation. To investigate the function of Cdh5 in sprout outgrowth, we generated null mutations in the zebrafish cdh5 gene, and we found that junctional remodeling and cell elongation are impaired in mutant embryos. The defects are associated with a disorganization of the actin cytoskeleton and cannot be rescued by expression of a truncated version of Cdh5. Finally, the defects in junctional remodeling can be phenocopied by pharmacological inhibition of actin polymerization, but not by inhibiting actin-myosin contractility. Taken together, our results support a model in which Cdh5 organizes junctional and cortical actin cytoskeletons, as well as provides structural support for polymerizing F-actin cables during endothelial cell elongation.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping