PSD-95 通过与 EB3 结合来改变微管动力学。
PSD-95 alters microtubule dynamics via an association with EB3.
机构信息
Department of Cell Biology and Neuroscience, Rutgers University, Piscataway, New Jersey 08854-8082, USA.
出版信息
J Neurosci. 2011 Jan 19;31(3):1038-47. doi: 10.1523/JNEUROSCI.1205-10.2011.
Abstract
Little is known about how the neuronal cytoskeleton is regulated when a dendrite decides whether to branch or not. Previously, we reported that postsynaptic density protein 95 (PSD-95) acts as a stop signal for dendrite branching. It is yet to be elucidated how PSD-95 affects the cytoskeleton and how this regulation relates to the dendritic arbor. Here, we show that the SH3 (src homology 3) domain of PSD-95 interacts with a proline-rich region within the microtubule end-binding protein EB3. Overexpression of PSD-95 or mutant EB3 results in a decreased lifetime of EB3 comets in dendrites. In line with these data, transfected rat neurons show that overexpression of PSD-95 results in less organized microtubules at dendritic branch points and decreased dendritogensis. The interaction between PSD-95 and EB3 elucidates a function for a novel region of EB3 and provides a new and important mechanism for the regulation of microtubules in determining dendritic morphology.
摘要
目前对于树突决定是否分支时神经元细胞骨架如何被调控知之甚少。我们先前的研究报道了突触后密度蛋白 95（PSD-95）作为树突分支的终止信号。目前仍不清楚 PSD-95 如何影响细胞骨架，以及这种调控与树突分支的关系。在这里，我们发现 PSD-95 的 SH3（src 同源 3）结构域与微管末端结合蛋白 EB3 内的一个富含脯氨酸的区域相互作用。PSD-95 的过表达或 EB3 的突变导致树突中 EB3 彗星的寿命缩短。与这些数据一致，转染的大鼠神经元显示 PSD-95 的过表达导致树突分支点处的微管组织减少，树突生成减少。PSD-95 和 EB3 之间的相互作用阐明了 EB3 的一个新的区域的功能，并为微管在决定树突形态中的调控提供了一个新的和重要的机制。
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