Ephrin-B2 forward signaling regulates somite patterning and neural crest cell development.
Genetic studies in the mouse have implicated ephrin-B2 (encoded by the gene Efnb2) in blood vessel formation, cardiac development and remodeling of the lymphatic vasculature. Here we report that loss of ephrin-B2 leads to defects in populations of cranial and trunk neural crest cells (NCC) and to defective somite development. In addition, we show that Efnb1/Efnb2 double heterozygous embryos exhibit phenotypes in a number of NCC derivatives. Expression of one copy of a mutant version of Efnb2 that lacks tyrosine phosphorylation sites was sufficient to rescue the embryonic phenotypes associated with loss of Efnb2. Our results uncover an important role for ephrin-B2 in NCC and somites during embryogenesis and suggest that ephrin-B2 exerts many of its embryonic function via activation of forward signaling.
Davy
Alice
A
Program in Developmental Biology, Division of Basic Sciences, Fred Hutchinson Cancer Research Center, 1100 Fairview Ave N., Seattle, WA 98109, USA.
Soriano
Philippe
P
D000818:Animals; D019521:Body Patterning / Q000502:physiology*; D017931:DNA Primers; D036388:Ephrin-B2 / Q000235:genetics / Q000378:metabolism*; D005455:Fluorescent Antibody Technique; D007150:Immunohistochemistry; D017403:In Situ Hybridization; D051379:Mice; D009432:Neural Crest / Q000502:physiology*; D015398:Signal Transduction / Q000502:physiology*; D019170:Somites / Q000502:physiology*
D017931:DNA Primers; D036388:Ephrin-B2