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Sec62通过依赖于UPR的ER-phagy限制了ER复制的正链RNA病毒感染

Ruiqi Wang¹, Qianshen Zhang¹, Lifan Zhou¹

¹State Key Laboratory of Plant Environmental Resilience, College of Biological Sciences, China Agricultural University, Beijing 100193, China.

|January 27, 2026

概括

甜菜黑烧病毒感染触发ER-phagy通过蛋白质p23和受体NbSec62.2. 这种宿主反应,即未折叠的蛋白质反应 (UPR),平衡病毒复制和内质网膜 (ER) 恒常性,限制其他 (+) RNA 病毒.

科学领域:

植物病毒学植物病毒学
分子植物-微生物相互作用
细胞平衡是细胞的平衡.

背景情况:

阳性链RNA[(+) RNA]病毒将宿主内膜重塑为病毒复制器官 (VRO),破坏细胞平衡.
宿主细胞恢复器官平衡的机制以及这如何影响病毒复制的机制尚未完全理解.

研究的目的:

为了研究宿主对 (+) RNA病毒诱导的内膜破坏的反应.
阐明内分泌网膜 (ER) 在抗病毒防御中的作用.
为了确定限制 (+) RNA 病毒复制的宿主因素.

主要方法:

使用甜菜黑烧病毒 (BBSV) 在Nicotiana benthamiana作为一个模型系统.
研究了BBSV蛋白p23与ER-phagy受体NbSec62.2.之间的相互作用.
分析了未折叠蛋白质响应 (UPR) 激活及其对ER-phagy和病毒复制的影响.

主要成果:

BBSV感染诱导ER-phagy,由病毒蛋白p23介导,与NbSec62.6相互作用.
在p23中的特定氨残留物 (F48) 对NbSec62相互作用和ER-phagy至关重要.
UPR激活促进病毒复制,但也触发了NbSec62-介导的ER-phagy以抑制BBSV.
NbSec62作为对其他ER复制 (+) RNA病毒 (如TMV和TuMV) 的限制因素.

结论:

NbSec62通过与病毒复制器官相互作用,作为对 (+) RNA 病毒的关键限制因子.
在感染期间,UPR-ER-phagy信号网络在平衡病毒复制和ER平衡中发挥着关键作用.
了解这个网络可以了解植物抗病毒防御策略.

关键词:

这是ER-phagy.阳性链RNA[(+) RNA]病毒第62章没有了甜菜黑烧病毒 (BBSV) 病毒细胞内膜网膜 (ER) 是一个复制复制复制复制复制复制复制限制因子的限制因子展开的蛋白质反应 (UPR)

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