Craniofacial defects in mice lacking BMP type I receptor Alk2 in neural crest cells

被引:187
作者
Dudas, M
Sridurongrit, S
Nagy, A
Okazaki, K
Kaartinen, V
机构
[1] Univ So Calif, Childrens Hosp Los Angeles, Keck Sch Med, Dev Biol Program,Dept Pathol, Los Angeles, CA 90027 USA
[2] Univ So Calif, Childrens Hosp Los Angeles, Keck Sch Med, Dev Biol Program,Dept Surg, Los Angeles, CA 90027 USA
[3] Biomol Engn Res Inst, Dept Mol Biol, Suita, Osaka 5650874, Japan
关键词
Alk2; bone morphogenetic protein; cleft palate; craniofacial neural crest; cranial bones; mandible; Meckel's cartilage; mental symphysis; temporomandibular joint;
D O I
10.1016/j.mod.2003.12.003
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
Neural crest cells (NCCs) are pluripotent migratory cells that contribute to the development of various craniofacial structures. Many signaling,molecules have been implicated in the formation, migration and differentiation of NCCs including bone morphogenetic proteins (BMPs). BMPs signal through a receptor complex composed of type I and type II receptors. Type I receptors (Alk2, Alk3 and AIk6) are the primary determinants of signaling specificity and therefore understanding their function is important in revealing the developmental roles of molecular pathways regulated by BMPs. Here we used a Cre/loxP system for neural crest specific deletion of AIk2. Our results show that mice - lacking Alk2 in the neural crest display multiple craniofacial defects including cleft palate and a hypotrophic mandible. Based on the present results we conclude that signaling via Alk2 receptors is non-redundant and regulates normal development of a restricted set of structures derived from the cranial neural crest. (C) 2004 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:173 / 182
页数:10
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