Craniofacial defects in mice lacking BMP type I receptor Alk2 in neural crest cells
Craniofacial defects in mice lacking BMP type I receptor Alk2 in neural crest cells
复制标题
DOI：
10.1016/j.mod.2003.12.003
复制
发表时间：
2004-02-01
影响因子：
2.6
通讯作者：
Kaartinen, V
中科院分区：
文献类型：
--
作者：
Dudas, M;Sridurongrit, S;Kaartinen, V
神经嵴细胞（NCC）是多能迁移细胞，有助于各种颅面结构的发育。许多信号分子参与了NCC的形成、迁移和分化，包括骨形态发生蛋白（BMP）。BMP通过由I型和II型受体组成的受体复合物发出信号。I型受体（Alk 2、Alk 3和Alk 6）是信号特异性的主要决定因素，因此了解它们的功能对于揭示BMP调节的分子途径的发育作用是重要的。在这里，我们使用Cre/loxP系统用于神经嵴特异性缺失AIk 2。我们的研究结果表明，神经嵴中缺乏Alk 2的小鼠表现出多种颅面缺陷，包括腭裂和下颌骨萎缩。基于目前的结果，我们得出结论，通过Alk 2受体的信号是非冗余的，并调节来自颅神经嵴的一组限制性结构的正常发育。(C)2004爱思唯尔爱尔兰有限公司保留所有权利。
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.