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番茄褪绿病毒 p22 与 NbBAG5 互作抑制自噬并调控病毒侵染。

Tomato chlorosis virus p22 interacts with NbBAG5 to inhibit autophagy and regulate virus infection.

机构信息

College of Plant Protection, Shandong Agricultural University, Tai'an, China.

State Key Laboratory of Crop Biology, College of Life Sciences, Shandong Agricultural University, Tai'an, China.

出版信息

Mol Plant Pathol. 2023 May;24(5):425-435. doi: 10.1111/mpp.13311. Epub 2023 Feb 24.

DOI:10.1111/mpp.13311
PMID:36828802
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10098061/
Abstract

Tomato chlorosis virus (ToCV) is a member of the genus Crinivirus in the family Closteroviridae. It has a wide host range and wide distribution, causing serious harm to the vegetable industry. The autophagy pathway plays an important role in plant resistance to virus infection. Viruses and plant hosts coevolve in defence and antidefence processes around autophagy. In this study, the interaction between ToCV p22 and Nicotiana benthamiana B-cell lymphoma2-associated athanogenes5 Nicotiana benthamiana (NbBAG5) was examined. Through overexpression and down-regulation of NbBAG5, results showed that NbBAG5 could negatively regulate ToCV infection. NbBAG5 was found to be localized in mitochondria and can change the original localization of ToCV p22, which is colocalized in mitochondria. NbBAG5 inhibited the expression of mitophagy-related genes and the number of autophagosomes, thereby regulating viral infection by affecting mitophagy. In summary, this study demonstrated that ToCV p22 affects autophagy by interacting with NbBAG5, established the association between viral infection, BAG proteins family, and the autophagy pathway, and explained the molecular mechanism by which ToCV p22 interacts with NbBAG5 to inhibit autophagy to regulate viral infection.

摘要

番茄褪绿病毒（ToCV）是棒状病毒科花椰菜花叶病毒属的成员。它具有广泛的宿主范围和广泛的分布，对蔬菜产业造成严重危害。自噬途径在植物抵抗病毒感染中起着重要作用。病毒和植物宿主在自噬周围的防御和反防御过程中共同进化。在这项研究中，研究了 ToCV p22 与拟南芥 B 细胞淋巴瘤 2 相关抗凋亡基因 5（Nicotiana benthamiana B-cell lymphoma 2-associated athanogenes5，NbBAG5）之间的相互作用。通过过表达和下调 NbBAG5，结果表明 NbBAG5 可以负调控 ToCV 感染。发现 NbBAG5 定位于线粒体中，并可以改变 ToCV p22 的原始定位，使其与线粒体共定位。NbBAG5 抑制了线粒体自噬相关基因的表达和自噬体的数量，从而通过影响线粒体自噬来调节病毒感染。总之，本研究表明，ToCV p22 通过与 NbBAG5 相互作用影响自噬，建立了病毒感染、BAG 蛋白家族和自噬途径之间的联系，并解释了 ToCV p22 与 NbBAG5 相互作用抑制自噬以调节病毒感染的分子机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1b22/10098061/ea1be32079ce/MPP-24-425-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1b22/10098061/dd4c84416747/MPP-24-425-g006.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1b22/10098061/d85834b57b04/MPP-24-425-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1b22/10098061/3c325ec72427/MPP-24-425-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1b22/10098061/ea1be32079ce/MPP-24-425-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1b22/10098061/dd4c84416747/MPP-24-425-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1b22/10098061/5063c495e985/MPP-24-425-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1b22/10098061/b0fdd4f56ce1/MPP-24-425-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1b22/10098061/d85834b57b04/MPP-24-425-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1b22/10098061/3c325ec72427/MPP-24-425-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1b22/10098061/ea1be32079ce/MPP-24-425-g005.jpg

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