• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

突触前自噬相关过程的组织

Organization of Presynaptic Autophagy-Related Processes.

作者信息

Gundelfinger Eckart D, Karpova Anna, Pielot Rainer, Garner Craig C, Kreutz Michael R

机构信息

Research Group Neuroplasticity, Leibniz Institute for Neurobiology, Magdeburg, Germany.

Institute of Pharmacology and Toxicology, Medical Faculty, Otto von Guericke University, Magdeburg, Germany.

出版信息

Front Synaptic Neurosci. 2022 Mar 17;14:829354. doi: 10.3389/fnsyn.2022.829354. eCollection 2022.

DOI:10.3389/fnsyn.2022.829354
PMID:35368245
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8968026/
Abstract

Brain synapses pose special challenges on the quality control of their protein machineries as they are far away from the neuronal soma, display a high potential for plastic adaptation and have a high energy demand to fulfill their physiological tasks. This applies in particular to the presynaptic part where neurotransmitter is released from synaptic vesicles, which in turn have to be recycled and refilled in a complex membrane trafficking cycle. Pathways to remove outdated and damaged proteins include the ubiquitin-proteasome system acting in the cytoplasm as well as membrane-associated endolysosomal and the autophagy systems. Here we focus on the latter systems and review what is known about the spatial organization of autophagy and endolysomal processes within the presynapse. We provide an inventory of which components of these degradative systems were found to be present in presynaptic boutons and where they might be anchored to the presynaptic apparatus. We identify three presynaptic structures reported to interact with known constituents of membrane-based protein-degradation pathways and therefore may serve as docking stations. These are (i) scaffolding proteins of the cytomatrix at the active zone, such as Bassoon or Clarinet, (ii) the endocytic machinery localized mainly at the peri-active zone, and (iii) synaptic vesicles. Finally, we sketch scenarios, how presynaptic autophagic cargos are tagged and recruited and which cellular mechanisms may govern membrane-associated protein turnover in the presynapse.

摘要

脑突触对其蛋白质机制的质量控制提出了特殊挑战,因为它们距离神经元胞体很远,具有高度的可塑性适应潜力,并且为完成其生理任务需要大量能量。这尤其适用于突触前部分,神经递质从突触小泡中释放出来,而突触小泡又必须在复杂的膜运输循环中进行回收和重新填充。清除过时和受损蛋白质的途径包括在细胞质中起作用的泛素-蛋白酶体系统以及与膜相关的内溶酶体和自噬系统。在这里,我们重点关注后一种系统,并综述关于突触前自噬和内溶酶体过程的空间组织的已知情况。我们列出了这些降解系统的哪些成分在突触前终扣中被发现,以及它们可能锚定在突触前装置的何处。我们确定了三个据报道与基于膜的蛋白质降解途径的已知成分相互作用、因此可能作为停靠站的突触前结构。它们是:(i)活性区细胞基质的支架蛋白,如巴松管蛋白或单簧管蛋白;(ii)主要位于活性区周围的内吞机制;(iii)突触小泡。最后,我们勾勒出突触前自噬货物如何被标记和募集的情景,以及哪些细胞机制可能控制突触前与膜相关的蛋白质周转。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7dad/8968026/88ce5565ed0d/fnsyn-14-829354-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7dad/8968026/51e0985e718b/fnsyn-14-829354-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7dad/8968026/14b81b7e3193/fnsyn-14-829354-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7dad/8968026/763a3901f358/fnsyn-14-829354-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7dad/8968026/694eeee5ca11/fnsyn-14-829354-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7dad/8968026/88ce5565ed0d/fnsyn-14-829354-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7dad/8968026/51e0985e718b/fnsyn-14-829354-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7dad/8968026/14b81b7e3193/fnsyn-14-829354-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7dad/8968026/763a3901f358/fnsyn-14-829354-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7dad/8968026/694eeee5ca11/fnsyn-14-829354-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7dad/8968026/88ce5565ed0d/fnsyn-14-829354-g005.jpg

相似文献

1
Organization of Presynaptic Autophagy-Related Processes.突触前自噬相关过程的组织
Front Synaptic Neurosci. 2022 Mar 17;14:829354. doi: 10.3389/fnsyn.2022.829354. eCollection 2022.
2
Autophagy and the endolysosomal system in presynaptic function.自噬和内溶酶体系统在突触前功能中的作用。
Cell Mol Life Sci. 2021 Mar;78(6):2621-2639. doi: 10.1007/s00018-020-03722-5. Epub 2020 Dec 19.
3
BSN (bassoon) and PRKN/parkin in concert control presynaptic vesicle autophagy.BSN(巴松管)和 PRKN/parkin 协同控制突触前囊泡自噬。
Autophagy. 2020 Sep;16(9):1732-1733. doi: 10.1080/15548627.2020.1801259. Epub 2020 Aug 10.
4
Bassoon Controls Presynaptic Autophagy through Atg5.巴松管通过 Atg5 控制突触自噬。
Neuron. 2017 Feb 22;93(4):897-913.e7. doi: 10.1016/j.neuron.2017.01.026.
5
Bassoon inhibits proteasome activity via interaction with PSMB4.巴松管通过与 PSMB4 相互作用抑制蛋白酶体活性。
Cell Mol Life Sci. 2021 Feb;78(4):1545-1563. doi: 10.1007/s00018-020-03590-z. Epub 2020 Jul 10.
6
Molecular organization and assembly of the presynaptic active zone of neurotransmitter release.神经递质释放的突触前活性区的分子组织与组装
Results Probl Cell Differ. 2006;43:49-68. doi: 10.1007/400_012.
7
Parkin contributes to synaptic vesicle autophagy in Bassoon-deficient mice.Parkin 参与了 Bassoon 缺失小鼠的突触囊泡自噬。
Elife. 2020 May 4;9:e56590. doi: 10.7554/eLife.56590.
8
Assembly of active zone precursor vesicles: obligatory trafficking of presynaptic cytomatrix proteins Bassoon and Piccolo via a trans-Golgi compartment.活性区前体囊泡的组装:突触前细胞基质蛋白巴松管和短笛通过反式高尔基体区室的必需运输。
J Biol Chem. 2006 Mar 3;281(9):6038-47. doi: 10.1074/jbc.M508784200. Epub 2005 Dec 21.
9
The presynaptic cytomatrix of brain synapses.脑突触的突触前细胞基质。
Cell Mol Life Sci. 2001 Jan;58(1):94-116. doi: 10.1007/PL00000781.
10
Bassoon and piccolo regulate ubiquitination and link presynaptic molecular dynamics with activity-regulated gene expression.巴松管蛋白和短笛蛋白调节泛素化,并将突触前分子动力学与活性调节基因表达联系起来。
J Physiol. 2016 Oct 1;594(19):5441-8. doi: 10.1113/JP271826. Epub 2016 Apr 24.

引用本文的文献

1
Synaptic sabotage: How Tau and α-Synuclein undermine synaptic health.突触破坏:tau蛋白和α-突触核蛋白如何损害突触健康。
J Cell Biol. 2025 Feb 3;224(2). doi: 10.1083/jcb.202409104. Epub 2024 Dec 24.
2
Neurons Specialize in Presynaptic Autophagy: A Perspective to Ameliorate Neurodegeneration.神经元在突触前自噬方面具有特异性:改善神经退行性变的一个视角。
Mol Neurobiol. 2025 Feb;62(2):2626-2640. doi: 10.1007/s12035-024-04399-8. Epub 2024 Aug 14.
3
S-SCAM is essential for synapse formation.S-SCAM对突触形成至关重要。

本文引用的文献

1
The active zone protein Clarinet regulates synaptic sorting of ATG-9 and presynaptic autophagy.活性带蛋白 Clarinet 调控 ATG-9 的突触分拣和突触前自噬。
PLoS Biol. 2023 Apr 13;21(4):e3002030. doi: 10.1371/journal.pbio.3002030. eCollection 2023 Apr.
2
Presynaptic autophagy is coupled to the synaptic vesicle cycle via ATG-9.突触前自噬通过 ATG-9 与突触囊泡循环偶联。
Neuron. 2022 Mar 2;110(5):824-840.e10. doi: 10.1016/j.neuron.2021.12.031. Epub 2022 Jan 21.
3
The ingenious ULKs: expanding the repertoire of the ULK complex with phosphoproteomics.
Front Cell Neurosci. 2023 Nov 16;17:1182493. doi: 10.3389/fncel.2023.1182493. eCollection 2023.
4
Oxysterols in Central and Peripheral Synaptic Communication.氧化甾醇在中枢和外周突触通讯中的作用。
Adv Exp Med Biol. 2024;1440:91-123. doi: 10.1007/978-3-031-43883-7_6.
5
ATG9 resides on a unique population of small vesicles in presynaptic nerve terminals.ATG9 位于突触前神经末梢的一小群独特小泡上。
Autophagy. 2024 Apr;20(4):883-901. doi: 10.1080/15548627.2023.2274204. Epub 2023 Nov 8.
6
Abl depletion via autophagy mediates the beneficial effects of quercetin against Alzheimer pathology across species.通过自噬介导的Abl缺失介导了槲皮素对跨物种阿尔茨海默病病理的有益作用。
Cell Death Discov. 2023 Oct 14;9(1):376. doi: 10.1038/s41420-023-01592-x.
7
Molecular Abnormalities in BTBR Mice and Their Relevance to Schizophrenia and Autism Spectrum Disorders: An Overview of Transcriptomic and Proteomic Studies.BTBR小鼠的分子异常及其与精神分裂症和自闭症谱系障碍的相关性:转录组学和蛋白质组学研究综述
Biomedicines. 2023 Jan 20;11(2):289. doi: 10.3390/biomedicines11020289.
具有创造力的 ULK 复合物:磷酸化蛋白质组学扩展 ULK 复合物的功能谱。
Autophagy. 2021 Dec;17(12):4491-4493. doi: 10.1080/15548627.2021.1968615. Epub 2021 Sep 14.
4
LRRK2 along the Golgi and lysosome connection: a jamming situation.LRRK2 在高尔基体和溶酶体连接中的作用:一种干扰情况。
Biochem Soc Trans. 2021 Nov 1;49(5):2063-2072. doi: 10.1042/BST20201146.
5
RUSC2 and WDR47 oppositely regulate kinesin-1-dependent distribution of ATG9A to the cell periphery.RUSC2 和 WDR47 反向调节依赖于驱动蛋白-1 的 ATG9A 向细胞边缘的分布。
Mol Biol Cell. 2021 Nov 1;32(21):ar25. doi: 10.1091/mbc.E21-06-0295. Epub 2021 Aug 25.
6
Who's in control? Principles of Rab GTPase activation in endolysosomal membrane trafficking and beyond.谁在掌控?Rab GTP 酶激活在内涵体膜运输及其他方面的原理。
J Cell Biol. 2021 Sep 6;220(9). doi: 10.1083/jcb.202105120. Epub 2021 Aug 12.
7
UBQLN proteins in health and disease with a focus on UBQLN2 in ALS/FTD.UBQLN 蛋白在健康和疾病中的作用,重点介绍 ALS/FTD 中的 UBQLN2。
FEBS J. 2022 Oct;289(20):6132-6153. doi: 10.1111/febs.16129. Epub 2021 Jul 28.
8
The Rab7 effector WDR91 promotes autophagy-lysosome degradation in neurons by regulating lysosome fusion.Rab7 效应因子 WDR91 通过调节溶酶体融合促进神经元中的自噬溶酶体降解。
J Cell Biol. 2021 Aug 2;220(8). doi: 10.1083/jcb.202007061. Epub 2021 May 24.
9
Sequential dynein effectors regulate axonal autophagosome motility in a maturation-dependent pathway.顺序动力蛋白效应器通过一种成熟依赖性途径调节轴突自噬体的运动。
J Cell Biol. 2021 Jul 5;220(7). doi: 10.1083/jcb.202010179. Epub 2021 May 20.
10
Atlastin 2/3 regulate ER targeting of the ULK1 complex to initiate autophagy.Atlastin 2/3 调节 ULK1 复合物向 ER 的靶向定位以启动自噬。
J Cell Biol. 2021 Jul 5;220(7). doi: 10.1083/jcb.202012091. Epub 2021 May 14.