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神经元树突中的Chaperone介导的自利用活动依赖的溶酶体外细胞分裂来处理蛋白质

Katarzyna M Grochowska¹, Marit Sperveslage¹, Rajeev Raman²

¹Leibniz Group "Dendritic Organelles and Synaptic Function," Center for Molecular Neurobiology, ZMNH, University Medical Center Hamburg-Eppendorf, 20251 Hamburg, Germany; Research Group Neuroplasticity, Leibniz Institute for Neurobiology, 39118 Magdeburg, Germany.

|August 17, 2023

概括

树突性溶解体通过外细胞突变 (exocytosis) 通过细胞外细胞突变释放蛋白质,这是NMDAR激活调节的过程. 这种途径有助于从神经元中清除有毒蛋白聚合物,如TDP-43.

科学领域:

神经科学是一个神经科学.
细胞生物学细胞生物学
蛋白质稳定性蛋白质稳定性

背景情况:

神经元复杂性挑战了蛋白质平衡 (蛋白质平衡).
lysosomal 降解机制主要在细胞 soma 中.
在树突中发现了成熟的溶酶体,能够进行细胞外释放.

研究的目的:

为了研究树突性溶解体的异质性和功能.
在树突中识别 lysosome exocytosis 的分子机制.
了解这个过程在清除容易聚合的蛋白质中的作用.

主要方法:

树突性 lysosome 组成的表征.
溶酶体相关膜蛋白 (LAMP) 2A和2B角色的分析.
研究溶解体与N-甲基-D-酸盐受体 (NMDARs) 之间的相互作用.
研究NMDAR激活对溶酶体运动性和融合的影响.
检查伴侣介导的自对外细胞形成的贡献.

主要成果:

树突性溶解体是异质的;只有LAMP2A/2B的溶解体表现出活动依赖的运动性和融合性.
LAMP2B调解了溶酶体对接到SAP102/Dlg3,这与含有GluN2B的NMDARs有关.
激活NMDAR可以降低溶酶体的运动性,并增强膜融合.
伴侣介导的自提供了溶酶体外细胞形成的内容.
这种机制有助于局部清除容易聚合的蛋白质 (例如,TDP-43,huntingtin).

结论:

树突性 lysosome exocytosis 是一个调节的过程,对神经元蛋白质稳定至关重要.
这条涉及LAMP2B和NMDARs的途径允许细胞外去除有毒蛋白质聚合物.
伴奏介导的自在为这种外细胞形成机制提供载荷方面发挥着关键作用.

关键词:

在CMA,CMA是CMA.CP: 细胞生物学细胞生物学科普:神经科学是什么意思在 GluN2B NMDAR 中.在LAMP2中使用LAMP2.这就是SAP102的原因.树突 (dendrites) 是一种树突.异位细胞形成的表细胞化.溶解体是溶解体的组成部分.

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