支持水疱性口腔炎病毒糖蛋白介导的融合的内泌体具有独特的运动和酸化。

IF 3.6 3区 生物学 Q3 CELL BIOLOGY
Traffic Pub Date : 2022-04-01 Epub Date: 2022-02-21 DOI:10.1111/tra.12836
Maya Cabot, Volker Kiessling, Judith M White, Lukas K Tamm
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引用次数: 2

摘要

大多数包膜病毒通过结合细胞表面的受体感染细胞,并通过内吞途径运输到具有触发与宿主内涵体膜融合的必要条件的隔室。内吞途径中的广泛类别包括早期和晚期内体,它们可以进一步分类为具有不同成熟率和运动特征的亚群。内分泌区室具有不同的蛋白质和脂质成分、管腔离子条件和pH值,为特定病毒的融合提供了独特的适宜环境。为了表征允许融合的区室,我们研究了表面带有水泡性口腔炎病毒糖蛋白(VSV-G)的假型病毒颗粒的运输和融合,并配备了一种新型pH传感器和荧光含量标记物,以测量活细胞中单个颗粒水平的pH、运动和融合。我们发现,VSV-G颗粒主要从酸性更强、活动性更强的内体融合,并且相当一部分颗粒被输送到不支持其融合的更静态、酸性更低的内体。此外,支持融合的内体进行定向运动。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Endosomes supporting fusion mediated by vesicular stomatitis virus glycoprotein have distinctive motion and acidification.

Most enveloped viruses infect cells by binding receptors at the cell surface and undergo trafficking through the endocytic pathway to a compartment with the requisite conditions to trigger fusion with a host endosomal membrane. Broad categories of compartments in the endocytic pathway include early and late endosomes, which can be further categorized into subpopulations with differing rates of maturation and motility characteristics. Endocytic compartments have varying protein and lipid components, luminal ionic conditions and pH that provide uniquely hospitable environments for specific viruses to fuse. In order to characterize compartments that permit fusion, we studied the trafficking and fusion of viral particles pseudotyped with the vesicular stomatitis virus glycoprotein (VSV-G) on their surface and equipped with a novel pH sensor and a fluorescent content marker to measure pH, motion and fusion at the single particle level in live cells. We found that the VSV-G particles fuse predominantly from more acidic and more motile endosomes, and that a significant fraction of particles is trafficked to more static and less acidic endosomes that do not support their fusion. Moreover, the fusion-supporting endosomes undergo directed motion.

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来源期刊
Traffic
Traffic 生物-细胞生物学
CiteScore
8.10
自引率
2.20%
发文量
50
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.
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