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疫霉属病原菌效应因子 Pi05910 抑制并破坏宿主乙醇酸氧化酶 StGOX4,从而促进植物易感性。

The Phytophthora infestans effector Pi05910 suppresses and destabilizes host glycolate oxidase StGOX4 to promote plant susceptibility.

机构信息

State Key Laboratory of Crop Stress Biology for Arid Areas and College of Agronomy, Northwest A&F University, Yangling, Shaanxi, China.

State Key Laboratory of Crop Stress Biology for Arid Areas and College of Plant Protection, Northwest A&F University, Yangling, Shaanxi, China.

出版信息

Mol Plant Pathol. 2024 Nov;25(11):e70021. doi: 10.1111/mpp.70021.

DOI:10.1111/mpp.70021
PMID:39487604
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11530570/
Abstract

Phytophthora infestans is a notorious oomycete pathogen that causes potato late blight. It secretes numerous effector proteins to manipulate host immunity. Understanding mechanisms underlying their host cell manipulation is crucial for developing disease resistance strategies. Here, we report that the conserved RXLR effector Pi05910 of P. infestans is a genotype-specific avirulence elicitor on potato variety Longshu 12 and contributes virulence by suppressing and destabilizing host glycolate oxidase StGOX4. By performing co-immunoprecipitation, yeast-two-hybrid assays, luciferase complementation imaging, bimolecular fluorescence complementation and isothermal titration calorimetry assays, we identified and confirmed potato StGOX4 as a target of Pi05910. Further analysis revealed that StGOX4 and its homologue NbGOX4 are positive immune regulators against P. infestans, as indicated by infection assays on potato and Nicotiana benthamiana overexpressing StGOX4 and TRV-NbGOX4 plants. StGOX4-mediated disease resistance involves enhanced reactive oxygen species accumulation and activated the salicylic acid signalling pathway. Pi05910 binding inhibited enzymatic activity and destabilized StGOX4. Furthermore, mutagenesis analyses indicated that the 25th residue (tyrosine, Y25) of StGOX4 mediates Pi05910 binding and is required for its immune function. Our results revealed that the core RXLR effector of P. infestans Pi05910 suppresses plant immunity by targeting StGOX4, which results in decreased enzymatic activity and protein accumulation, leading to enhanced plant susceptibility.

摘要

致病疫霉是一种臭名昭著的卵菌病原体,可引起马铃薯晚疫病。它分泌许多效应蛋白来操纵宿主的免疫。了解其宿主细胞操纵的机制对于开发抗病策略至关重要。在这里,我们报告称,致病疫霉的保守 RXLR 效应子 Pi05910 是马铃薯品种龙薯 12 的基因型特异性无毒诱导子,通过抑制和破坏宿主乙醇酸氧化酶 StGOX4 来发挥毒性。通过进行共免疫沉淀、酵母双杂交测定、荧光素酶互补成像、双分子荧光互补和等温滴定量热法测定,我们鉴定并确认了马铃薯 StGOX4 是 Pi05910 的靶标。进一步的分析表明,StGOX4及其同源物 NbGOX4 是针对致病疫霉的正向免疫调节因子,这表现在马铃薯和拟南芥上过表达 StGOX4 和 TRV-NbGOX4 植物的感染测定中。StGOX4 介导的抗病性涉及活性氧物质的积累增加和水杨酸信号通路的激活。Pi05910 的结合抑制了酶活性并破坏了 StGOX4。此外,突变分析表明,StGOX4 的第 25 位残基(酪氨酸,Y25)介导了 Pi05910 的结合,并且对于其免疫功能是必需的。我们的结果表明,致病疫霉的核心 RXLR 效应子 Pi05910 通过靶向 StGOX4 抑制植物免疫,从而导致酶活性降低和蛋白积累减少,导致植物易感性增强。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6505/11530570/f738de638623/MPP-25-e70021-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6505/11530570/c652c53b05da/MPP-25-e70021-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6505/11530570/57536cdcfecd/MPP-25-e70021-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6505/11530570/f03900edee9d/MPP-25-e70021-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6505/11530570/68afdc1eb5a3/MPP-25-e70021-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6505/11530570/75c93152549a/MPP-25-e70021-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6505/11530570/f738de638623/MPP-25-e70021-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6505/11530570/c652c53b05da/MPP-25-e70021-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6505/11530570/57536cdcfecd/MPP-25-e70021-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6505/11530570/f03900edee9d/MPP-25-e70021-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6505/11530570/68afdc1eb5a3/MPP-25-e70021-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6505/11530570/75c93152549a/MPP-25-e70021-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6505/11530570/f738de638623/MPP-25-e70021-g002.jpg

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