A role of MAP1B in Reelin-dependent neuronal migration
A role of MAP1B in Reelin-dependent neuronal migration
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DOI：
10.1093/cercor/bhh213
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发表时间：
2005-08-01
期刊：
影响因子：
3.7
通讯作者：
Avila, J
中科院分区：
文献类型：
--
作者：
González-Billault, C;Del Río, JA;Avila, J
控制神经元迁移的信号级联被认为是将细胞外信号与细胞骨架成分联系起来。MAP1B是一种神经元特异性微管相关蛋白，参与微管动态稳定性的控制以及微管与肌动蛋白丝之间的相互作用。在这里，我们表明，Reelin可以诱导模式I MAP1B磷酸化，在体内和体外，通过GSK3和CDK5激活。此外，mDab1参与负责模式I MAP1B磷酸化的信号级联。相反，MAP1B缺陷小鼠显示神经系统的异常结构，特别是在脑分层区域，表明神经元迁移失败。因此，我们提出，Reelin可以诱导MAP1B的翻译后修饰，这可能与其在神经元迁移中的功能相关。
The signaling cascades governing neuronal migration are believed to link extracellular signals to cytoskeletal components. MAP1B is a neuron-specific microtubule-associated protein implicated in the control of the dynamic stability of microtubules and in the cross-talk between microtubules and actin filaments. Here we show that Reelin can induce mode I MAP1B phosphorylation, both in vivo and in vitro, through gsk3 and cdk5 activation. Additionally, mDab1 participates in the signaling cascade responsible for mode I MAP1B phosphorylation. Conversely, MAP1B-deficient mice display an abnormal structuring of the nervous system, especially in brain laminated areas, indicating a failure in neuronal migration. Therefore, we propose that Reelin can induce post-translational modifications on MAP1B that could correlate with its function in neuronal migration.