致病疫霉无毒效应子 Avr3b 的单个区域在细胞死亡诱导和植物免疫抑制中起作用,Molecular Plant Pathology

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致病疫霉无毒效应子 Avr3b 的单个区域在细胞死亡诱导和植物免疫抑制中起作用
Molecular Plant Pathology ( IF 4.8 ) Pub Date : 2023-01-25 , DOI: 10.1111/mpp.13298
Biao Gu ₁ , Wenxin Gao ₁ , Zeqi Liu ₁ , Guangda Shao ₁ , Qin Peng ₁ , Yinyu Mu ₁ , Qinhu Wang ₁ , Hua Zhao ₁ , Jianqiang Miao ₁ , Xili Liu ₁

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作为一种破坏性植物病原体，致病疫霉分泌多种进入宿主的 RxLR 效应子以促进感染。一种关键的 RxLR 效应子 PiAvr3b 不仅诱导与马铃薯抗性蛋白 StR3b 相关的效应子触发免疫 (ETI)，而且抑制病原体相关分子模式 (PAMP) 触发的免疫 (PTI)。迄今为止，这种双重活动背后的分子基础仍然未知。基于全球致病疫霉的系统发育分析分离株，我们发现了两个 PiAvr3b 亚型，它们相差三个氨基酸。尽管存在这种序列差异，但两种亚型在激活 StR3b 介导的超敏反应 (HR) 和抑制由三种 PAMP（PiNpp、PiINF1 和 PsXeg1）和一个 RxLR 效应子 (Pi10232) 诱导的坏死方面保持相同的特性。使用联合诱变方法，我们发现 PiAvr3b 的双重活性紧密相连，并由 C 末端的 88 个氨基酸决定。我们进一步确定 PiAvr3b 的 W60 或 E134 残基对于触发 StR3b 相关的 HR 和抑制 PiNpp 和 Pi10232 相关的坏死是必不可少的，而 S99 残基部分有助于 PTI 抑制。此外，需要 PiAvr3b 的核定位来刺激 HR 和抑制 PTI，而不是抑制 Pi10232 相关细胞死亡。

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A single region of the Phytophthora infestans avirulence effector Avr3b functions in both cell death induction and plant immunity suppression

As a destructive plant pathogen, Phytophthora infestans secretes diverse host-entering RxLR effectors to facilitate infection. One critical RxLR effector, PiAvr3b, not only induces effector-triggered immunity (ETI), which is associated with the potato resistance protein StR3b, but also suppresses pathogen-associated molecular pattern (PAMP)-triggered immunity (PTI). To date, the molecular basis underlying such dual activities remains unknown. Based on phylogenetic analysis of global P. infestans isolates, we found two PiAvr3b isoforms that differ by three amino acids. Despite this sequence variation, the two isoforms retain the same properties in activating the StR3b-mediated hypersensitive response (HR) and inhibiting necrosis induced by three PAMPs (PiNpp, PiINF1, and PsXeg1) and an RxLR effector (Pi10232). Using a combined mutagenesis approach, we found that the dual activities of PiAvr3b were tightly linked and determined by 88 amino acids at the C-terminus. We further determined that either the W60 or the E134 residue of PiAvr3b was essential for triggering StR3b-associated HR and inhibiting PiNpp- and Pi10232-associated necrosis, while the S99 residue partially contributed to PTI suppression. Additionally, nuclear localization of PiAvr3b was required to stimulate HR and suppress PTI, but not to inhibit Pi10232-associated cell death. Our study revealed that PiAvr3b suppresses the plant immune response at different subcellular locations and provides an example in which a single amino acid of an RxLR effector links ETI induction and cell death suppression.

更新日期：2023-01-25

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