ATG9 promotes autophagosome formation through interaction with LC3

IF 2.5 3区 生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY Biochemical and biophysical research communications Pub Date : 2025-02-02 DOI:10.1016/j.bbrc.2024.151254
Peiqi Xu , Ting Zhang , Fangfang Yu , Lixia Guo , Yanan Yang
{"title":"ATG9 promotes autophagosome formation through interaction with LC3","authors":"Peiqi Xu ,&nbsp;Ting Zhang ,&nbsp;Fangfang Yu ,&nbsp;Lixia Guo ,&nbsp;Yanan Yang","doi":"10.1016/j.bbrc.2024.151254","DOIUrl":null,"url":null,"abstract":"<div><div>The autophagosome is a double-membrane organelle that executes macroautophagy. Previous studies have shown that the autophagosome formation is driven by autophagy-related genes, among which ATG9 is the only conserved transmembrane protein and has been shown to play a critical role in the autophagosome formation. However, how ATG9 binds to the growing autophagosome membrane has remained uncertain. Herein, we report that ATG9 binds to LC3, an essential membrane component of the autophagosome, thereby allowing ATG9 to incorporate into the autophagosome membrane. Mechanistically, we show that ATG9 interacts with LC3 through its UIM motives, which bind to the UDS site of LC3. Interrupting such UIM-UDS interaction abolishes the autophagosome association of ATG9 and suppresses the autophagosome formation. Collectively, our findings reveal a novel mechanism regulating autophagosome biogenesis and suggest that the interaction of ATG9 with LC3 is critical for ATG9 binding to the growing autophagosome membrane.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"747 ","pages":"Article 151254"},"PeriodicalIF":2.5000,"publicationDate":"2025-02-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Biochemical and biophysical research communications","FirstCategoryId":"99","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0006291X2401790X","RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}
引用次数: 0

Abstract

The autophagosome is a double-membrane organelle that executes macroautophagy. Previous studies have shown that the autophagosome formation is driven by autophagy-related genes, among which ATG9 is the only conserved transmembrane protein and has been shown to play a critical role in the autophagosome formation. However, how ATG9 binds to the growing autophagosome membrane has remained uncertain. Herein, we report that ATG9 binds to LC3, an essential membrane component of the autophagosome, thereby allowing ATG9 to incorporate into the autophagosome membrane. Mechanistically, we show that ATG9 interacts with LC3 through its UIM motives, which bind to the UDS site of LC3. Interrupting such UIM-UDS interaction abolishes the autophagosome association of ATG9 and suppresses the autophagosome formation. Collectively, our findings reveal a novel mechanism regulating autophagosome biogenesis and suggest that the interaction of ATG9 with LC3 is critical for ATG9 binding to the growing autophagosome membrane.
查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
ATG9通过与LC3相互作用促进自噬体的形成。
自噬体是一种执行巨噬的双膜细胞器。以往的研究表明,自噬体的形成是由自噬相关基因驱动的,其中ATG9是唯一保守的跨膜蛋白,在自噬体的形成中起关键作用。然而,ATG9如何与生长中的自噬体膜结合仍不确定。本文中,我们报道ATG9与LC3结合,LC3是自噬体的重要膜组分,从而使ATG9结合到自噬体膜中。在机制上,我们发现ATG9通过其UIM动机与LC3相互作用,该动机结合到LC3的UDS位点。中断这种UIM-UDS相互作用可消除ATG9的自噬体关联并抑制自噬体的形成。总之,我们的研究结果揭示了一种调节自噬体生物发生的新机制,并表明ATG9与LC3的相互作用对于ATG9与生长中的自噬体膜结合至关重要。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 去求助
来源期刊
Biochemical and biophysical research communications
Biochemical and biophysical research communications 生物-生化与分子生物学
CiteScore
6.10
自引率
0.00%
发文量
1400
审稿时长
14 days
期刊介绍: Biochemical and Biophysical Research Communications is the premier international journal devoted to the very rapid dissemination of timely and significant experimental results in diverse fields of biological research. The development of the "Breakthroughs and Views" section brings the minireview format to the journal, and issues often contain collections of special interest manuscripts. BBRC is published weekly (52 issues/year).Research Areas now include: Biochemistry; biophysics; cell biology; developmental biology; immunology ; molecular biology; neurobiology; plant biology and proteomics
期刊最新文献
Editorial Board OsMADS22 interacts with OsMADS50 to regulate floral transition in rice Unspliced XBP1 enhences metabolic reprogramming in colorectal cancer cells by interfering with the mitochondrial localization of MGME1 Editorial Board Corrigendum to "Soyasapogenol c: A novel liver x receptor α agonist that mitigates cholesterol accumulation in diabetic kidney disease" [Biochem. Biophys. Res. Commun. 752 (2025) 151366].
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1