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SEC31a-ATG9a 相互作用介导 COPII 囊泡招募用于自噬体形成。

SEC31a-ATG9a Interaction Mediates the Recruitment of COPII Vesicles for Autophagosome Formation.

机构信息

Key Laboratory of Shaanxi Province for Craniofacial Precision Medicine Research, College of Stomatology, Xi'an Jiaotong University, Xi'an, Shaanxi, 710004, China.

Department of Oral Sciences, Faculty of Dentistry, University of Otago, Dunedin, 9016, New Zealand.

出版信息

Adv Sci (Weinh). 2024 Nov;11(44):e2405127. doi: 10.1002/advs.202405127. Epub 2024 Oct 3.

DOI:10.1002/advs.202405127
PMID:39361436
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11600210/
Abstract

Autophagy plays an important role in determining stem-cell differentiation. During the osteogenic differentiation of mesenchymal stem cells (MSCs), autophagosome formation is upregulated but the reason is unknown. A long-standing quest in the autophagy field is to find the membrane origin of autophagosomes. In this study, cytoplasmic coat protein complex II (COPII) vesicles, endoplasmic reticulum-derived vesicles responsible for the transport of storage proteins to the Golgi, are demonstrated to be a critical source of osteoblastic autophagosomal membrane. A significant correlation between the number of COPII vesicle and the autophagy level is identified in the rat bone tissues. Disruption of COPII vesicles restrained osteogenesis and decreased the number and size of autophagosomes. SEC31a (an outer coat protein of COPII vesicle) is found to be vital to regulate COPII vesicle-dependent autophagosome formation via interacting with ATG9a of autophagosomal seed vesicles. The interference of Sec31a inhibited autophagosome formation and osteogenesis in vitro and in vivo. These results identified a novel mechanism of autophagosome formation in osteogenic differentiation of stem cells and identified SEC31a as a critical protein that mediates the interplay between COPII and ATG9a vesicles. These findings broaden the understanding of the regulatory mechanism in the osteogenic differentiation of MSCs.

摘要

自噬在决定干细胞分化中起着重要作用。在间充质干细胞（MSCs）的成骨分化过程中，自噬体的形成被上调，但原因尚不清楚。自噬领域的一个长期探索目标是寻找自噬体的膜起源。在这项研究中，证明细胞质被膜蛋白复合物 II（COPII）小泡（负责将储存蛋白运输到高尔基体的内质网衍生小泡）是成骨细胞自噬体膜的关键来源。在大鼠骨组织中，鉴定出 COPII 小泡的数量与自噬水平之间存在显著相关性。COPII 小泡的破坏抑制成骨作用，并减少自噬体的数量和大小。发现 SEC31a（COPII 小泡的外被膜蛋白）对于通过与自噬体种子小泡的 ATG9a 相互作用来调节 COPII 小泡依赖性自噬体形成至关重要。Sec31a 的干扰抑制了体外和体内的自噬体形成和成骨作用。这些结果确定了干细胞成骨分化中自噬体形成的新机制，并确定 SEC31a 是介导 COPII 和 ATG9a 小泡相互作用的关键蛋白。这些发现拓宽了对 MSCs 成骨分化调控机制的理解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/534f/11600210/b7e21fb67528/ADVS-11-2405127-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/534f/11600210/3b2ecbe79577/ADVS-11-2405127-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/534f/11600210/cec109a70cb3/ADVS-11-2405127-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/534f/11600210/407f1cd822f9/ADVS-11-2405127-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/534f/11600210/80179559b3d7/ADVS-11-2405127-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/534f/11600210/9ddee5e5faea/ADVS-11-2405127-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/534f/11600210/3bb3d4bd46d0/ADVS-11-2405127-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/534f/11600210/b7e21fb67528/ADVS-11-2405127-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/534f/11600210/3b2ecbe79577/ADVS-11-2405127-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/534f/11600210/cec109a70cb3/ADVS-11-2405127-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/534f/11600210/407f1cd822f9/ADVS-11-2405127-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/534f/11600210/80179559b3d7/ADVS-11-2405127-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/534f/11600210/9ddee5e5faea/ADVS-11-2405127-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/534f/11600210/3bb3d4bd46d0/ADVS-11-2405127-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/534f/11600210/b7e21fb67528/ADVS-11-2405127-g002.jpg

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