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21 Eph receptors and ephrins control the morphogenesis of limbs and blood vessels.

The large family of Eph receptors and their cell-surface-bound ephrin ligands are versatile regulators of numerous processes during embryonic morphogenesis. Two molecular subgroups can be distinguished based on structure, sequence homology, and binding affinity. Glycosyl phosphatidylinositol (GPI) anchored ephrin-A ligands bind to EphA receptors whereas ephrin-B ligands, transmembrane proteins with a highly conserved cyto-plasmic tail, interact with EphB receptors. Previous work has demonstrated that ephrins have the remarkable ability to mediate receptor-like signalling resulting in bidirectional signal transduction. 
 
We have recently shown that endothelial cells express the two B-class ligands ephrin-B1 and ephrin-B2. Indicating important roles in blood vessel morphogenesis, both molecules can induce endothelial sprouting in vitro. This was further supported by the finding that angiogenesis and certain aspects of vasculogenesis are disrupted in mutant mice lacking ephrin-B2. To study the in vivo function of ephrin-B2 in more detail, we generated tissue-specific (Cre-loxP) mutant mice. Our phenotypic analysis indicates that mutant embryos with both complete or endothelial cell-specific inactivation of the ephrin-B2 gene show very similar defects and that ephrin-B2 is indispensable on the endothelial lining of blood vessels. 
 
Targeted inactivation of the X-linked ephrin-B1 gene also resulted in embryonic lethality due to a range of different defects. Null mutant mice developed extensive oedema in the back region suggesting malformation/malfunction of the cardiovascular or the lymphatic system. As one of the two X-chromosomes is randomly inactivated at the blastocyst stage and all progeny of a cell inherits the pattern of X-inactivation, heterozygous female embryos are mosaic with tissue patches using either the wild-type or the knockout ephrin-B1 allele. Remarkably, heterozygous females but not hemizyous knockout males display preaxial polydactyly. Our results suggest that interaction between ephrin-B1 and its B-class Eph receptors control patterning of the limb bud.