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Complete ablation of ephrin-B1 resulted in perinatal lethality associated with a range of phenotypes, including defects in neural crest cell (NCC)-derived tissues, incomplete body wall closure, and abnormal skeletal patterning. Conditional deletion of ephrin-B1 demonstrated that ephrin-B1 acts autonomously in NCCs, and controls their migration. Last, a mutation in the PDZ binding domain indicated that ephrin-B1-induced reverse signaling is required in NCCs. Our results demonstrate that ephrin-B1 acts both as a ligand and as a receptor in a tissue-specific manner during embryogenesis.<\/jats:p>","DOI":"10.1101\/gad.1171704","type":"journal-article","created":{"date-parts":[[2004,3,22]],"date-time":"2004-03-22T18:30:55Z","timestamp":1079980255000},"page":"572-583","source":"Crossref","is-referenced-by-count":254,"title":["Ephrin-B1 forward and reverse signaling are required during mouse 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