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Targeted disruption of semaphorin 3C leads to persistent truncus arteriosus and aortic arch interruption

¹ Department of Neuroscience, University of Pennsylvania School of Medicine, 1115 BRB II/III, 421 Curie Blvd, Philadelphia, PA 19104, USA
² Department of Medicine, Cardiovascular Division, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA
³ The Rockefeller University, New York, New York 10021, USA
^* Author for correspondence (e-mail:raperj{at}mail.med.upen.edu )

Accepted 31 May 2001

Semaphorin 3C is a secreted member of the semaphorin gene family. To investigate its function in vivo, we have disrupted the semaphorin 3C locus in mice by targeted mutagenesis. semaphorin 3C mutant mice die within hours after birth from congenital cardiovascular defects consisting of interruption of the aortic arch and improper septation of the cardiac outflow tract. This phenotype is similar to that reported following ablation of the cardiac neural crest in chick embryos and resembles congenital heart defects seen in humans. Semaphorin 3C is expressed in the cardiac outflow tract as neural crest cells migrate into it. Their entry is disrupted in semaphorin 3C mutant mice. These data suggest that semaphorin 3C promotes crest cell migration into the proximal cardiac outflow tract.

Key words: Semaphorin 3C, Mouse, Cardiac neural crest, Interrupted aortic arch, Persistent truncus arteriosus, PlexinA2, Chemoattractant, Sema3C

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