病原体效应因子BcSSP2抑制了NPC相位分离,以促进Botrytis cinerea感染
Jiaojiao Wang1,2, Dewei Wu3,4, Gaofeng Pei5
1College of Biological Sciences and Biotechnology, Beijing Forestry University, Beijing, China. nxywjj@163.com.
Nature communications
|September 29, 2025
概括
病原体作用者可以通过破坏生物分子相分离来抑制植物免疫力. 一种Botrytis cinerea效应剂,BcSSP2,向核孔综合体 (NPC),抑制宿主防御并促进感染.
科学领域:
- 植物病理学 植物病理学
- 分子生物学分子生物学
- 免疫学 免疫学 免疫学
背景情况:
- 生物分子相位分离对于植物和动物免疫是至关重要的.
- 病原体作用者旨在克服宿主防御,以成功感染.
- 众所周知,很少有植物病原体影响者能够准相位分离介导免疫.
研究的目的:
- 通过破坏相分离来抑制植物免疫力的病原体效应因子的识别和表征.
- 调查这种效应器干扰宿主防御通路的机制.
- 探索这种策略在病原体中的进化保存.
主要方法:
- 来自 Botrytis cinerea 的效应蛋白 BcSSP2 的鉴定.
- 研究BcSSP2与植物核孔综合体 (NPC) 的相互作用.
- 分析BcSSP2对NUP62相隔离和MPK3核传输的影响.
- 在其他死菌虫中对BcSSP2同类的比较分析.
主要成果:
- BcSSP2, Botrytis cinerea 的一个效应体,破坏了 NUP62 在植物 NPC 的相分离.
- 这种干扰抑制了免疫调节器MPK3的核运输,抑制了植物的防御.
- BcSSP2同类物在死菌性菌体中广泛存在,并且也破坏了NUP62相分离.
结论:
- 破坏植物NPC相位分离是一种由死菌病原体使用的进化保守策略.
- BcSSP2通过NPC相分离干扰抑制宿主免疫力来促进Botrytis cinerea感染.
- 这项研究揭示了一种新的病原体毒性机制,针对宿主相隔离动态.
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