TLS-GFP cannot rescue mRNP formation near spines and spine phenotype in TLS-KO
TLS-GFP cannot rescue mRNP formation near spines and spine phenotype in TLS-KO
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DOI：
10.1097/wnr.0b013e32831bedb0
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发表时间：
2009-01-07
期刊：
影响因子：
1.7
通讯作者：
Takumi, Toru
中科院分区：
文献类型：
--
作者：
Fujii, Ritsuko;Grossenbacher-Zinchuk, Olga;Takumi, Toru
RNA结合蛋白TLS将编码肌动蛋白稳定蛋白的Nd 1-L mRNA转运至神经元树突。TLS-null小鼠（TLS-KO）海马神经元显示异常的棘形态，因此可以归因于肌动蛋白不稳定的Nd 1-L mRNA的树突供应不当。在这项研究中，我们表明，TLS的外源性表达在TLS-KO神经元没有拯救异常的脊柱表型。外源性TLS和Nd 1-LmRNA在TLS-KO神经元树突和棘中的共定位程度显著降低。我们的研究结果表明，TLS-Nd 1-L mRNA复合物簇的形成，推测mRNA池的本地蛋白质合成的脊髓，在TLS-deficient神经元受损。NeuroReport 20：57-61（C）2009年沃尔特斯·克鲁沃健康垂直酒吧Lippincott威廉姆斯&威尔金斯。
RNA-binding protein TLS transports Nd1-L mRNA, which encodes an actin-stabilizing protein, to the neuronal dendrites. TLS-null mouse (TLS-KO) hippocampal neurons display abnormal spine morphology, and thus could be attributed to actin destabilization by the improper supply of Nd1-L mRNA to the dendrites. In this study, we showed that the exogenous expression of TLS in TLS-KO neurons did not rescue the abnormal spine phenotypes. The degree of colocalization between exogenous TLS and Nd1-L mRNA was significantly decreased in both the neuronal dendrites and the spines of TLS-KO neurons. Our results indicate that formation of TLS-Nd1-L mRNA complex clusters, presumable mRNA pools for the local protein synthesis in the spines, was impaired in TLS-deficient neurons. NeuroReport 20:57-61 (C) 2009 Wolters Kluwer Health vertical bar Lippincott Williams & Wilkins.