SUMOylation of spastin promotes the internalization of GluA1 and regulates dendritic spine morphology by targeting microtubule dynamics
SUMOylation of spastin promotes the internalization of GluA1 and regulates dendritic spine morphology by targeting microtubule dynamics
复制标题
spastin 的 SUMO 化促进 GluA1 的内化并通过靶向微管动力学调节树突棘形态
DOI：
10.1016/j.nbd.2020.105133
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发表时间：
2020-12-01
影响因子：
6.1
通讯作者：
Guo, Guo-Qing
中科院分区：
文献类型：
--
作者：
Ji, Zhi-Sheng;Liu, Qiu-Ling;Guo, Guo-Qing
树突棘是参与兴奋性突触接触发生的神经元过程的特化结构。微管细胞骨架对于维持棘形态和成熟突触至关重要。Spastin与微管切断蛋白酶有关，并参与突触终扣的形成。然而，目前尚不清楚痉挛蛋白是否可以被小泛素样修饰物（SUMO）修饰，或者这种修饰如何调节树突棘。Spastin在K427处被SUMO化，其去SUMO化促进微管稳定性。此外，痉挛素的SUMO化被证明影响与长期突触抑制相关的信号通路。SUMO化的spastin促进树突和树突棘的发育。此外，SUMO化的痉挛调节内吞作用，并影响AMPA受体，GluA1的运输。我们的研究结果表明，SUMO化的痉挛促进GluA1的内化和调节树突棘形态通过靶向微管动力学。
Dendritic spines are specialized structures involved in neuronal processes on which excitatory synaptic contact occurs. The microtubule cytoskeleton is vital for maintaining spine morphology and mature synapses. Spastin is related to microtubule-severing proteases and is involved in synaptic bouton formation. However, it is not yet known if spastin can be modified by Small Ubiquitin-like Modifier (SUMO) or how this modification regulates dendritic spines. Spastin was shown to be SUMOylated at K427, and its deSUMOylation promoted microtubule stability. In addition, SUMOylation of spastin was shown to affect signalling pathways associated with long term synaptic depression. SUMOylated spastin promoted the development of dendrites and dendritic spines. Moreover, SUMOylated spastin regulated endocytosis and affected the transport of the AMPA receptor, GluA1. Our findings suggest that SUMOylation of spastin promotes GluA1 internalization and regulates dendritic spine morphology through targeting of microtubule dynamics.