Phospholipase D and retromer promote recycling of TRPL ion channel via the endoplasmic reticulum.

IF 3.6 3区 生物学 Q3 CELL BIOLOGY
Traffic Pub Date : 2022-01-01 Epub Date: 2021-11-10 DOI:10.1111/tra.12824
Krystina Wagner, Thomas K Smylla, Marko Lampe, Jana Krieg, Armin Huber
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引用次数: 1

Abstract

Plasma membrane protein trafficking is of fundamental importance for cell function and cell integrity of neurons and includes regulated protein recycling. In this work, we report a novel role of the endoplasmic reticulum (ER) for protein recycling as discovered in trafficking studies of the ion channel TRPL in photoreceptor cells of Drosophila. TRPL is located within the rhabdomeric membrane from where it is endocytosed upon light stimulation and stored in the cell body. Conventional immunohistochemistry as well as stimulated emission depletion super-resolution microscopy revealed TRPL storage at the ER after illumination, suggesting an unusual recycling route of TRPL. Our results also imply that both phospholipase D (PLD) and retromer complex are required for correct recycling of TRPL to the rhabdomeric membrane. Loss of PLD activity in PLD3.1 mutants results in enhanced degradation of TRPL. In the retromer mutant vps35MH20 , TRPL is trapped in a Rab5-positive compartment. Evidenced by epistatic analysis in the double mutant PLD3.1 vps35MH20 , PLD activity precedes retromer function. We propose a model in which PLD and retromer function play key roles in the transport of TRPL to an ER enriched compartment.

磷脂酶D和逆转录酶通过内质网促进TRPL离子通道的再循环。
质膜蛋白转运对神经元的细胞功能和细胞完整性至关重要,包括调节蛋白质的再循环。在这项工作中,我们报告了在果蝇感光细胞中离子通道TRPL的运输研究中发现的内质网(ER)在蛋白质循环中的新作用。TRPL位于横纹肌膜内,在光刺激下被内吞并储存在细胞体中。常规免疫组织化学和刺激发射耗尽超分辨显微镜显示,光照后,TRPL储存在内质网,提示TRPL的循环途径不寻常。我们的结果还表明,磷脂酶D (PLD)和反转录复合物都需要TRPL到横纹肌膜的正确再循环。PLD3.1突变体PLD活性的丧失导致TRPL降解增强。在逆转录突变体vps35MH20中,TRPL被困在rab5阳性的隔室中。双突变体PLD3.1 vps35MH20的上位分析证明,PLD活性先于逆转录功能。我们提出了一个模型,其中PLD和后转录功能在TRPL转运到ER富集室中起关键作用。
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
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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