SWIP介导WASH复合物的逆转录酶非依赖性膜募集。

IF 3.6 3区 生物学 Q3 CELL BIOLOGY
Traffic Pub Date : 2023-05-01 Epub Date: 2023-03-30 DOI:10.1111/tra.12884
Vojtěch Dostál, Tereza Humhalová, Pavla Beránková, Ondřej Pácalt, Lenka Libusová
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引用次数: 2

摘要

五聚体WASH复合物通过激活Arp2/3促进内体蛋白质分选,这反过来又导致在内体表面形成特异性的F-肌动蛋白斑块。通常认为,WASH复合物通过其亚基FAM21与逆转录酶亚基VPS35的相互作用附着在内涵体膜上。然而,我们观察到即使在没有VPS35的情况下,WASH复合物和F-肌动蛋白也存在于内体上。我们发现WASH复合物以反转录物依赖性和反转录物非依赖性的方式与内体表面结合。反转录酶非依赖性膜锚是由SWIP亚基直接介导的。此外,SWIP可以与许多磷酸肌醇物种相互作用。其中,我们的数据表明,与磷脂酰肌醇-3,5-二磷酸(PI(3,5)P2)的相互作用对SWIP的内体结合至关重要。总的来说,这项研究揭示了讲卫生运动复合体亚单位SWIP的新作用,并强调讲卫生运动综合体是一个独立、自给自足的贩运监管机构。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

SWIP mediates retromer-independent membrane recruitment of the WASH complex.

SWIP mediates retromer-independent membrane recruitment of the WASH complex.

The pentameric WASH complex facilitates endosomal protein sorting by activating Arp2/3, which in turn leads to the formation of F-actin patches specifically on the endosomal surface. It is generally accepted that WASH complex attaches to the endosomal membrane via the interaction of its subunit FAM21 with the retromer subunit VPS35. However, we observe the WASH complex and F-actin present on endosomes even in the absence of VPS35. We show that the WASH complex binds to the endosomal surface in both a retromer-dependent and a retromer-independent manner. The retromer-independent membrane anchor is directly mediated by the subunit SWIP. Furthermore, SWIP can interact with a number of phosphoinositide species. Of those, our data suggest that the interaction with phosphatidylinositol-3,5-bisphosphate (PI(3,5)P2 ) is crucial to the endosomal binding of SWIP. Overall, this study reveals a new role of the WASH complex subunit SWIP and highlights the WASH complex as an independent, self-sufficient trafficking regulator.

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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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