LKB1 signaling in cephalic neural crest cells is essential for vertebrate head development
LKB1 signaling in cephalic neural crest cells is essential for vertebrate head development
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DOI：
10.1016/j.ydbio.2016.08.006
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发表时间：
2016-10-15
影响因子：
2.7
通讯作者：
Billaud, Marc
中科院分区：
文献类型：
--
作者：
Creuzet, Sophie E.;Viallet, Jean P.;Billaud, Marc
脊椎动物的头部发育是通过一系列复杂的模式机制和包括头神经嵴细胞（CNCC）在内的细胞间相互作用进行的。这些细胞从神经管背缘分离后，沿着固定的路径进行广泛的迁移，形成了大部分颅面骨骼。在这里，我们报道LKB1肿瘤抑制因子的沉默会影响迁移前CNCC从神经原基的分层，以及它们的极化和存活，从而导致严重的面部和脑部缺陷。我们进一步表明，lkb1介导的CNCC的发展涉及amp激活的蛋白激酶（AMPK）、rho依赖性激酶（ROCK）和基于肌动蛋白的运动蛋白myosin II的顺序激活。总之，这些结果表明，控制头部形成的复杂形态发生过程严重依赖于CNCC中LKB1信号网络的激活。(C) 2016 Elsevier Inc.版权所有。
Head development in vertebrates proceeds through a series of elaborate patterning mechanisms and cell-cell interactions involving cephalic neural crest cells (CNCC). These cells undergo extensive migration along stereotypical paths after their separation from the dorsal margins of the neural tube and they give rise to most of the craniofacial skeleton. Here, we report that the silencing of the LKB1 tumor suppressor affects the delamination of pre-migratory CNCC from the neural primordium as well as their polarization and survival, thus resulting in severe facial and brain defects. We further show that LKB1-mediated effects on the development of CNCC involve the sequential activation of the AMP-activated protein kinase (AMPK), the Rho-dependent kinase (ROCK) and the actin-based motor protein myosin II. Collectively, these results establish that the complex morphogenetic processes governing head formation critically depends on the activation of the LKB1 signaling network in CNCC. (C) 2016 Elsevier Inc. All rights reserved.