双子病毒效应器AC4通过Upf1降解抑制了无意中介的mRNA衰变
Shuangqin Bai1,2, Haiyan Wang1,3, Qiuxian Xie1,2
1State Key Laboratory of Tropical Crop Breeding, Institute of Tropical Bioscience and Biotechnology, Chinese Academy of Tropical Agricultural Sciences, Sanya/Haikou, Hainan, China.
Plant, cell & environment
|February 22, 2026
概括
斯里兰卡麻豆马赛克病毒AC4蛋白降解宿主因子Upf1,抑制无意义介导的mRNA衰变 (NMD) 抗病毒防御. 这种病毒策略增强了病毒积累和病原性.
科学领域:
- 植物病毒相互作用
- RNA生物学的RNA生物学
- 宿主蛋白质稳定作用 宿主蛋白质稳定作用
背景情况:
- 无意中介的mRNA衰变 (NMD) 是一种关键的RNA监测途径和抗病毒防御机制.
- 双子病毒,一组DNA病毒,拥有逃避宿主抗病毒反应的机制,但这些尚未完全理解.
研究的目的:
- 调查斯里兰卡麻豆马赛克病毒 (SLCMV) AC4蛋白如何对抗NMD途径.
- 阐明SLCMV AC4抑制NMD的分子机制及其对病毒病原性的影响.
主要方法:
- 利用尼科蒂亚娜·本塔米亚纳和阿拉比多普西斯·塔利亚纳的模型来研究SLCMV AC4蛋白功能.
- 使用结合试验研究了SLCMV AC4和宿主因子Upf1之间的相互作用.
- 分析了Upf1枯竭中涉及的降解途径 (自和无素蛋白酶体).
- 进行了AC4 N-终端基化基因的结构和功能分析.
- 研究了AC4对内源性NMD基质和异质病毒积累的影响.
主要成果:
- 在SLCMV中,AC4蛋白向并降低NMD中央调节器Upf1.1.
- AC4通过其N端域直接与AtUpf1结合,通过自和无素-蛋白酶体通路启动降解.
- AC4的N-终端基化动机对于NMD抑制和Upf1降解至关重要.
- AC4表达稳定了NMD基质,并增强了异种病毒的积累和致病性.
- AC4通过破坏GAPC2-ATG3相互作用来激活自,促进自细胞形成.
结论:
- 通过降低宿主RNA监视因子Upf1.1,SLCMV采用了一种复杂的反防御策略.
- AC4蛋白的N端密里斯基基化基因在调节Upf1降解中起着至关重要的作用.
- 这种机制突出显示了病毒效应因子,RNA生物学和宿主蛋白质稳定之间的新型相互作用,影响了病毒的致病性.
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