RalA and the exocyst complex influence neuronal polarity through PAR-3 and aPKC
RalA and the exocyst complex influence neuronal polarity through PAR-3 and aPKC
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DOI：
10.1242/jcs.044339
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发表时间：
2009-05-15
影响因子：
4
通讯作者：
Lalli, Giovanna
中科院分区：
文献类型：
--
作者：
Lalli, Giovanna
神经元极化需要局部的细胞骨架变化和极化膜传输。在这里，我报告小GTPase RalA，先前显示控制神经突分支，也调节神经元极性。在培养的神经元中，RalA耗竭或组成活性RalA的异位表达会抑制轴突的形成。然而，不能与胞囊复合物相互作用的组成活性RalA突变体的表达对神经元极化没有影响。此外，胞囊复合体的Sec6、Sec8或Exo84亚基的耗竭也会导致神经元无极化。神经元极化的早期阶段伴随着胞囊复合物与PAR-3和非典型蛋白激酶C （aPKC）相互作用水平的增加，以及胞囊复合物与PAR-3的rala依赖性关联。因此，神经元极化涉及一种由rala调节的囊泡运输介质（胞囊复合物）和细胞极性（PAR-3）之间的关联。
Neuronal polarization requires localized cytoskeletal changes and polarized membrane traffic. Here, I report that the small GTPase RalA, previously shown to control neurite branching, also regulates neuronal polarity. RalA depletion, or ectopic expression of constitutively active RalA in cultured neurons inhibit axon formation. However, expression of a constitutively active RalA mutant that is unable to interact with the exocyst complex has no effect on neuronal polarization. Furthermore, depletion of the Sec6, Sec8 or Exo84 subunits of the exocyst complex also leads to unpolarized neurons. Early stages of neuronal polarization are accompanied by increasing levels of interaction of the exocyst complex with PAR-3 and atypical protein kinase C (aPKC), and by the RalA-dependent association of the exocyst complex with PAR-3. Thus, neuronal polarization involves a RalA-regulated association between mediators of vesicle trafficking (exocyst complex) and cell polarity (PAR-3).