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神经蛋白2通过Drosophila中的RACK1-cofilin信号传递来控制突触形态和功能

Yichen Sun^1,2, Moyi Li^3,4, Junhua Geng¹

¹School of Life Science and Technology, The Key Laboratory of Developmental Genes and Human Disease, Southeast University, Nanjing, 210096, China.

Communications biology

|October 18, 2023

概括

神经蛋白-2 (DNlg2) 通过RACK1和Cofilin在Drosophila神经肌肉结节的信号传递来调节actin细胞骨架的组装. 这条通路对于突触结构,功能和运动至关重要.

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
生物化学生物化学

背景情况:

神经原蛋白是细胞粘附蛋白,与自闭症谱系障碍有关.
它们在调节actin细胞骨中的作用尚未完全理解.
了解这些机制是神经连接研究的关键.

研究的目的:

研究神经蛋白调节actin细胞骨架的因素和机制.
在这个过程中识别神经蛋白的新型相互作用伙伴.
阐明DNlg2在神经肌肉结合处的actin动态中的作用.

主要方法:

使用Drosophila神经肌肉结 (NMJ) 作为模型系统.
研究了DNlg2,RACK1和Cofilin信号传递之间的相互作用.
分析了dnlg2突变体中的actin细胞骨恒温,NMJ结构,突触传输和运动.
评估了可菲林操纵 (过度表达/无活化) 对已获救的突变表型的影响.

主要成果:

发现了Drosophila Neuroligin-2 (DNlg2) 和RACK1之间的一种新型相互作用,它调解了Cofilin信号传递.
DNlg2的删除破坏了RACK1-Cofilin通路,导致NMJ的actin细胞骨架稳定性受损.
dnlg2突变体表现出异常的NMJ结构,降低了突触传输和异常的幼虫运动.
过度表达野生型或激活的Cofilin挽救了这些缺陷,而非激活的Cofilin没有.

结论:

DNlg2通过Drosophila NMJ的RACK1-Cofilin通路协调F-actin的组合.
这条通路对于维持突触结构,功能和运动行为至关重要.
神经原蛋白介导的活性蛋白调节是一个多样化的过程,不同的神经原蛋白利用不同的机制 (例如,DNlg1通过WAVE复合体).

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