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Defective ALK5 signaling in the neural crest leads to increased postmigratory neural crest cell apoptosis and severe outflow tract defects Wang J; Nagy A; Larsson J; Dudas M; Sucov HM; Kaartinen VBMC Dev Biol 2006[Nov]; 6 (�): 51BACKGROUND: Congenital cardiovascular diseases are the most common form of birth defects in humans. A substantial portion of these defects has been associated with inappropriate induction, migration, differentiation and patterning of pluripotent cardiac neural crest stem cells. While TGF-beta-superfamily signaling has been strongly implicated in neural crest cell development, the detailed molecular signaling mechanisms in vivo are still poorly understood. RESULTS: We deleted the TGF-beta type I receptor Alk5 specifically in the mouse neural crest cell lineage. Failure in signaling via ALK5 leads to severe cardiovascular and pharyngeal defects, including inappropriate remodeling of pharyngeal arch arteries, abnormal aortic sac development, failure in pharyngeal organ migration and persistent truncus arteriosus. While ALK5 is not required for neural crest cell migration, our results demonstrate that it plays an important role in the survival of post-migratory cardiac neural crest cells. CONCLUSION: Our results demonstrate that ALK5-mediated signaling in neural crest cells plays an essential cell-autonomous role in the pharyngeal and cardiac outflow tract development.|Activin Receptors, Type I/*deficiency/genetics/physiology[MESH]|Animals[MESH]|Aorta/abnormalities/embryology[MESH]|Apoptosis/*genetics[MESH]|Branchial Region/abnormalities/embryology[MESH]|Cell Movement/*genetics[MESH]|Female[MESH]|Heart Defects, Congenital/embryology/*genetics[MESH]|Mice[MESH]|Mice, Knockout[MESH]|Mice, Transgenic[MESH]|Neural Crest/*embryology/*pathology[MESH]|Protein Serine-Threonine Kinases[MESH]|Receptor, Transforming Growth Factor-beta Type I[MESH]|Receptors, Transforming Growth Factor beta/*deficiency/genetics/physiology[MESH]|Signal Transduction/*genetics[MESH] |