The COPII coat protein SEC24D is required for autophagosome closure in mammals.

IF 3.5 4区 生物学 Q1 Biochemistry, Genetics and Molecular Biology
Tianlong He, Cuicui Ji, Wenting Zhang, Xianghua Li, Yukun Liu, Xiaoli Wang, Haolin Zhang, Juan Wang
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引用次数: 0

Abstract

Macroautophagy involves the encapsulation of cellular components within double-membrane autophagosomes for subsequent degradation in vacuoles or lysosomes. Coat protein complex II (COPII) vesicles serve as a membrane source for autophagosome formation. However, the specific role of SEC24D, an isoform of the COPII coat protein SEC24, in the macroautophagy pathway remains unclear. In this study, we demonstrate that SEC24D is indispensable for macroautophagy and important for autophagosome closure. Depletion of SEC24D leads to the accumulation of unsealed isolation membranes. Furthermore, under conditions of starvation, SEC24D interacts with casein kinase1 delta (CK1δ), a member of the casein kinase 1 family, and autophagy-related 9A (ATG9A). Collectively, our findings unveil the indispensable role of SEC24D in starvation-induced autophagy in mammalian cells.

哺乳动物的自噬体关闭需要 COPII 外壳蛋白 SEC24D。
大自噬是指将细胞成分包裹在双膜自噬体中,随后在液泡或溶酶体中降解。衣壳蛋白复合体 II(COPII)囊泡是自噬体形成的膜源。然而,COPII衣壳蛋白SEC24的异构体SEC24D在大自噬途径中的具体作用仍不清楚。在这项研究中,我们证明了SEC24D对于大自噬是不可或缺的,而且对于自噬体的闭合也很重要。消耗 SEC24D 会导致未封闭的隔离膜的积累。此外,在饥饿条件下,SEC24D 与酪蛋白激酶 1 家族成员酪蛋白激酶 1 delta(CK1δ)和自噬相关 9A(ATG9A)相互作用。总之,我们的研究结果揭示了 SEC24D 在哺乳动物细胞饥饿诱导的自噬中不可或缺的作用。
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
FEBS Letters
FEBS Letters 生物-生化与分子生物学
CiteScore
7.00
自引率
2.90%
发文量
303
审稿时长
1.0 months
期刊介绍: FEBS Letters is one of the world''s leading journals in molecular biology and is renowned both for its quality of content and speed of production. Bringing together the most important developments in the molecular biosciences, FEBS Letters provides an international forum for Minireviews, Research Letters and Hypotheses that merit urgent publication.
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