Pcdh11x Negatively Regulates Dendritic Branching
Pcdh11x Negatively Regulates Dendritic Branching
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Pcdh11x 负向调节树突分支
DOI：
10.1007/s12031-015-0515-8
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发表时间：
2015-08-01
影响因子：
3.1
通讯作者：
Xu, Ruxiang
中科院分区：
文献类型：
--
作者：
Wu, Cuiying;Niu, Lijun;Xu, Ruxiang
神经元树突分支的正确形成对正确的大脑功能至关重要。感受性突触接触的数量和分布由树枝的大小和形状决定。我们先前的研究发现，原钙粘蛋白11 X连锁蛋白(Pcdh11x)主要在神经元中表达，并对树突状分支有影响。在这项研究中，功能获得和功能丧失实验表明，Pcdh11x对培养的胚胎第16天小鼠皮质神经元的树突分支起负调节作用。野生型Pcdh11x(Pcdh11x-GFP)的过表达降低了树突的复杂性，而Pcdh11x的敲除增加了树突的分枝。进一步证明，Pcdh11x激活PI3K/AKT信号通路，负向调节树突分支。
Proper formation of neuronal dendritic branching is crucial for correct brain function. The number and distribution of receptive synaptic contacts are defined by the size and shape of dendritic arbors. Our previous research found that protocadherin 11 X-linked protein (Pcdh11x) is predominantly expressed in neurons and has an influence on dendritic branching. In this study, gain-of-function and loss-of-function experiments revealed that Pcdh11x acts as a negative regulator of dendritic branching in cultured cortical neurons derived from embryonic day 16 mice. Overexpression of wild-type Pcdh11x (Pcdh11x-GFP) reduced dendritic complexity, whereas knockdown of Pcdh11x increased dendritic branching. It was further demonstrated that Pcdh11x activates PI3K/AKT signaling to negatively regulate dendritic branching.