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YIPF3 和 YIPF4 调节高尔基体的自噬性周转。

YIPF3 and YIPF4 regulate autophagic turnover of the Golgi apparatus.

机构信息

Department of Genetics, Graduate School of Medicine, Osaka University, Suita, Osaka, 565-0871, Japan.

Integrated Frontier Research for Medical Science Division, Institute for Open and Transdisciplinary Research Initiatives (OTRI), Osaka University, Suita, Osaka, 565-0871, Japan.

出版信息

EMBO J. 2024 Jul;43(14):2954-2978. doi: 10.1038/s44318-024-00131-3. Epub 2024 May 31.

DOI:10.1038/s44318-024-00131-3
PMID:38822137
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11250848/
Abstract

The degradation of organelles by autophagy is essential for cellular homeostasis. The Golgi apparatus has recently been demonstrated to be degraded by autophagy, but little is known about how the Golgi is recognized by the forming autophagosome. Using quantitative proteomic analysis and two novel Golgiphagy reporter systems, we found that the five-pass transmembrane Golgi-resident proteins YIPF3 and YIPF4 constitute a Golgiphagy receptor. The interaction of this complex with LC3B, GABARAP, and GABARAPL1 is dependent on a LIR motif within YIPF3 and putative phosphorylation sites immediately upstream; the stability of the complex is governed by YIPF4. Expression of a YIPF3 protein containing a mutated LIR motif caused an elongated Golgi morphology, indicating the importance of Golgi turnover via selective autophagy. The reporter assays reported here may be readily adapted to different experimental contexts to help deepen our understanding of Golgiphagy.

摘要

自噬作用导致细胞器降解对于细胞内稳态至关重要。最近已经证明高尔基体可以被自噬作用降解，但是对于高尔基体如何被正在形成的自噬体识别，人们知之甚少。通过定量蛋白质组学分析和两种新型的高尔基体自噬报告系统，我们发现五次跨膜高尔基体驻留蛋白 YIPF3 和 YIPF4 构成了高尔基体自噬受体。该复合物与 LC3B、GABARAP 和 GABARAPL1 的相互作用依赖于 YIPF3 内的 LIR 基序和上游的假定磷酸化位点；复合物的稳定性由 YIPF4 控制。表达含有突变 LIR 基序的 YIPF3 蛋白会导致高尔基体形态拉长，表明通过选择性自噬进行高尔基体周转的重要性。这里报道的报告实验可以很容易地适应不同的实验环境，以帮助我们更深入地了解高尔基体自噬。

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2
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Nat Rev Genet. 2023 Jun;24(6):382-400. doi: 10.1038/s41576-022-00562-w. Epub 2023 Jan 12.
3
A pulse-chasable reporter processing assay for mammalian autophagic flux with HaloTag.一种使用 HaloTag 进行哺乳动物自噬流的脉冲可捕获报告者处理测定法。
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Biochem Soc Trans. 2024 Apr 24;52(2):581-592. doi: 10.1042/BST20230316.
4
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Elife. 2022 Aug 8;11:e78923. doi: 10.7554/eLife.78923.
4
Identification of a Golgi-localized peptide reveals a minimal Golgi-targeting motif.鉴定一种高尔基定位肽揭示了一个最小的高尔基靶向基序。
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5
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6
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