title: Distinct and redundant functions of Esama and VE-cadherin during vascular morphogenesis.
abstract: The cardiovascular system forms during early embryogenesis and adapts to embryonic growth by sprouting angiogenesis and vascular remodeling. These processes require fine-tuning of cell-cell adhesion to maintain and re-establish endothelial contacts, while allowing cell motility. We have compared the contribution of two endothelial cell-specific adhesion proteins, VE-cadherin (VE-cad/Cdh5) and Esama (endothelial cell-selective adhesion molecule a), during angiogenic sprouting and blood vessel fusion (anastomosis) in the zebrafish embryo by genetic analyses. Different combinations of mutant alleles can be placed into a phenotypic series with increasing defects in filopodial contact formation. Contact formation inesamamutants appears similar to wild type, whereasesama-/-;ve-cad+/-andve-cadsingle mutants exhibit intermediate phenotypes. The lack of both proteins interrupts filopodial interaction completely. Furthermore, double mutants do not form a stable endothelial monolayer, and display intrajunctional gaps, dislocalization of Zo-1 and defects in apical-basal polarization. In summary, VE-cadherin and Esama have distinct and redundant functions during blood vessel morphogenesis, and both adhesion proteins are central to endothelial cell recognition during anastomosis.
authors.affiliation: Biozentrum der Universität Basel, Klingelbergstrasse 70, Basel CH-4056, Switzerland.
authors.forename: Loïc
authors.initials: L
authors.lastname: Sauteur
authors.affiliation: Biozentrum der Universität Basel, Klingelbergstrasse 70, Basel CH-4056, Switzerland markus.affolter@unibas.ch heinz-georg.belting@unibas.ch.
authors.forename: Markus
authors.initials: M
authors.lastname: Affolter
authors.affiliation: Biozentrum der Universität Basel, Klingelbergstrasse 70, Basel CH-4056, Switzerland markus.affolter@unibas.ch heinz-georg.belting@unibas.ch.
authors.forename: Heinz-Georg
authors.identifier: 0000-0002-1538-4364
authors.initials: HG
authors.lastname: Belting
mesh_terms: D000818:Animals; D015703:Antigens, CD / Q000378:metabolism*; D001808:Blood Vessels / Q000196:embryology* / Q000378:metabolism*; D015820:Cadherins / Q000378:metabolism*; D015815:Cell Adhesion Molecules / Q000378:metabolism*; D002450:Cell Communication; D016764:Cell Polarity; D042783:Endothelial Cells / Q000166:cytology / Q000378:metabolism; D007365:Intercellular Junctions / Q000378:metabolism; D009024:Morphogenesis; D009154:Mutation / Q000235:genetics; D018919:Neovascularization, Physiologic; D011554:Pseudopodia / Q000378:metabolism; D015027:Zebrafish / Q000196:embryology* / Q000378:metabolism*; D029961:Zebrafish Proteins / Q000378:metabolism*; D000099152:Cadherin 5
chemical_list: D015703:Antigens, CD; D015820:Cadherins; D015815:Cell Adhesion Molecules; D029961:Zebrafish Proteins; D000099152:Cadherin 5
keywords: Anastomosis; Angiogenesis; Cdh5; Cell adhesion; Cell contact formation; Endothelial cell; Esam; Morphogenesis; VE-cadherin; Zebrafish