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突触素与突触结合蛋白之间的多价静电 π-阳离子相互作用是凝聚的原因。

Multivalent electrostatic pi-cation interaction between synaptophysin and synapsin is responsible for the coacervation.

机构信息

Department of Physiology and Biomedical Sciences, Seoul National University College of Medicine, Seoul, 03080, South Korea.

UK Dementia Research Institute, University College London, Cruciform Building, Gower St, London, WC1E 6BT, UK.

出版信息

Mol Brain. 2021 Sep 8;14(1):137. doi: 10.1186/s13041-021-00846-y.

Abstract

We recently showed that synaptophysin (Syph) and synapsin (Syn) can induce liquid-liquid phase separation (LLPS) to cluster small synaptic-like microvesicles in living cells which are highly reminiscent of SV cluster. However, as there is no physical interaction between them, the underlying mechanism for their coacervation remains unknown. Here, we showed that the coacervation between Syph and Syn is primarily governed by multivalent pi-cation electrostatic interactions among tyrosine residues of Syph C-terminal (Ct) and positively charged Syn. We found that Syph Ct is intrinsically disordered and it alone can form liquid droplets by interactions among themselves at high concentration in a crowding environment in vitro or when assisted by additional interactions by tagging with light-sensitive CRY2PHR or subunits of a multimeric protein in living cells. Syph Ct contains 10 repeated sequences, 9 of them start with tyrosine, and mutating 9 tyrosine to serine (9YS) completely abolished the phase separating property of Syph Ct, indicating tyrosine-mediated pi-interactions are critical. We further found that 9YS mutation failed to coacervate with Syn, and since 9YS retains Syph's negative charge, the results indicate that pi-cation interactions rather than simple charge interactions are responsible for their coacervation. In addition to revealing the underlying mechanism of Syph and Syn coacervation, our results also raise the possibility that physiological regulation of pi-cation interactions between Syph and Syn during synaptic activity may contribute to the dynamics of synaptic vesicle clustering.

摘要

我们最近表明,突触小泡相关蛋白(Syph)和突触结合蛋白(Syn)可以诱导液-液相分离(LLPS),从而在活细胞中聚集类似小突触囊泡的小囊泡,这非常类似于 SV 簇。然而,由于它们之间没有物理相互作用,其凝聚的潜在机制尚不清楚。在这里,我们表明,Syph 和 Syn 之间的凝聚主要受 Syph C 端(Ct)酪氨酸残基与带正电荷的 Syn 之间的多价 pi-阳离子静电相互作用控制。我们发现,Syph Ct 本质上是无序的,它可以在体外高浓度拥挤环境中通过自身相互作用,或在添加光敏 CRY2PHR 标记或活细胞中多聚体蛋白亚基的额外相互作用的辅助下,单独形成液滴。Syph Ct 包含 10 个重复序列,其中 9 个以酪氨酸开始,将 9 个酪氨酸突变为丝氨酸(9YS)完全消除了 Syph Ct 的相分离特性,表明酪氨酸介导的 pi 相互作用至关重要。我们进一步发现,9YS 突变不能与 Syn 凝聚,并且由于 9YS 保留了 Syph 的负电荷,结果表明 pi-阳离子相互作用而不是简单的电荷相互作用是导致它们凝聚的原因。除了揭示 Syph 和 Syn 凝聚的潜在机制外,我们的结果还提出了这样一种可能性,即在突触活动期间,Syph 和 Syn 之间的 pi-阳离子相互作用的生理调节可能有助于突触囊泡聚集的动力学。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ebc9/8424992/4081d7f2442a/13041_2021_846_Fig1_HTML.jpg

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