Acute COG complex inactivation unveiled its immediate impact on Golgi and illuminated the nature of intra-Golgi recycling vesicles.

IF 3.6 3区生物学 Q3 CELL BIOLOGY

Traffic Pub Date : 2023-02-01 Epub Date: 2022-12-15 DOI:10.1111/tra.12876

Farhana Taher Sumya, Irina D Pokrovskaya, Zinia D'Souza, Vladimir V Lupashin

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引用次数: 0

Abstract

Conserved Oligomeric Golgi (COG) complex controls Golgi trafficking and glycosylation, but the precise COG mechanism is unknown. The auxin-inducible acute degradation system was employed to investigate initial defects resulting from COG dysfunction. We found that acute COG inactivation caused a massive accumulation of COG-dependent (CCD) vesicles that carry the bulk of Golgi enzymes and resident proteins. v-SNAREs (GS15, GS28) and v-tethers (giantin, golgin84, and TMF1) were relocalized into CCD vesicles, while t-SNAREs (STX5, YKT6), t-tethers (GM130, p115), and most of Rab proteins remained Golgi-associated. Airyscan microscopy and velocity gradient analysis revealed that different Golgi residents are segregated into different populations of CCD vesicles. Acute COG depletion significantly affected three Golgi-based vesicular coats-COPI, AP1, and GGA, suggesting that COG uniquely orchestrates tethering of multiple types of intra-Golgi CCD vesicles produced by different coat machineries. This study provided the first detailed view of primary cellular defects associated with COG dysfunction in human cells.

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急性 COG 复合物失活揭示了它对高尔基体的直接影响，并阐明了高尔基体内循环囊泡的性质。

保守寡聚高尔基体（COG）复合物控制着高尔基体的贩运和糖基化，但COG的确切机制尚不清楚。我们采用了辅助素诱导的急性降解系统来研究 COG 功能障碍导致的初始缺陷。我们发现，COG 急性失活会导致 COG 依赖性（CCD）囊泡大量聚集，这些囊泡携带了大部分高尔基体酶和常驻蛋白。v-SNAREs（GS15、GS28）和 v-tethers（giantin、golgin84 和 TMF1）重新定位到 CCD 囊泡中，而 t-SNAREs （STX5、YKT6）、t-tethers（GM130、p115）和大部分 Rab 蛋白仍与高尔基体相关。空气扫描显微镜和速度梯度分析表明，不同的高尔基居民被分离到不同的 CCD 囊泡群中。急性COG耗竭显著影响了三种基于高尔基体的囊泡包被--COPI、AP1和GGA，表明COG独特地协调了由不同包被机制产生的多种类型的高尔基体内CCD囊泡的系链。这项研究首次详细揭示了人类细胞中与 COG 功能障碍相关的主要细胞缺陷。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Traffic 生物-细胞生物学

CiteScore

8.10

自引率

2.20%

发文量

审稿时长

2 months

期刊介绍： Traffic encourages and facilitates the publication of papers in any field relating to intracellular transport in health and disease. Traffic papers span disciplines such as developmental biology, neuroscience, innate and adaptive immunity, epithelial cell biology, intracellular pathogens and host-pathogen interactions, among others using any eukaryotic model system. Areas of particular interest include protein, nucleic acid and lipid traffic, molecular motors, intracellular pathogens, intracellular proteolysis, nuclear import and export, cytokinesis and the cell cycle, the interface between signaling and trafficking or localization, protein translocation, the cell biology of adaptive an innate immunity, organelle biogenesis, metabolism, cell polarity and organization, and organelle movement. All aspects of the structural, molecular biology, biochemistry, genetics, morphology, intracellular signaling and relationship to hereditary or infectious diseases will be covered. Manuscripts must provide a clear conceptual or mechanistic advance. The editors will reject papers that require major changes, including addition of significant experimental data or other significant revision. Traffic will consider manuscripts of any length, but encourages authors to limit their papers to 16 typeset pages or less.