RXLR effectors from Phytophthora infestans suppress host cell death and promote virulence via nuclear localization in Nicotiana benthamiana

IF 4.1 2区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY
SangA Park , Taewon Kim , Soeui Lee , Ye-Eun Seo , Solhee In , Doil Choi , Joo Hyun Lee
{"title":"RXLR effectors from Phytophthora infestans suppress host cell death and promote virulence via nuclear localization in Nicotiana benthamiana","authors":"SangA Park ,&nbsp;Taewon Kim ,&nbsp;Soeui Lee ,&nbsp;Ye-Eun Seo ,&nbsp;Solhee In ,&nbsp;Doil Choi ,&nbsp;Joo Hyun Lee","doi":"10.1016/j.plantsci.2025.112730","DOIUrl":null,"url":null,"abstract":"<div><div><em>Phytophthora infestans</em>, a destructive hemibiotrophic pathogen, relies on effector proteins to modulate host immunity and facilitate infection. However, the molecular mechanisms by which these effectors suppress host cell death during the biotrophic phase remain poorly understood. In this study, we identified three RXLR effectors—designated as Cell Death Suppressors (CDS1: Pi02860, CDS2: Pi04089, and CDS5: Pi06099)—that strongly suppress effector-triggered cell death in <em>Nicotiana benthamiana</em>. These CDSs are highly expressed during the early biotrophic phase and inhibit cell death triggered by diverse elicitors, including INF1, NPP1.1, Rpiblb2/Avrblb2, and Avr3a/R3a. Subcellular localization analysis revealed that the nuclear targeting is essential for their cell death suppressive activity. Functional assays demonstrated that CDS1 significantly enhances <em>P. infestans</em> virulence, while CDS2 and CDS5 contribute synergistically when co-expressed. Moreover, homologs of CDS1 from other <em>Phytophthora</em> species exhibited similar suppressive activity, despite lacking obvious sequence or structural features predictive of function. Our findings suggest that <em>P. infestans</em> utilizes a coordinated set of nuclear-targeting effectors to suppress host immunity during early colonization, offering new insights into pathogen strategies for immune evasion.</div></div>","PeriodicalId":20273,"journal":{"name":"Plant Science","volume":"362 ","pages":"Article 112730"},"PeriodicalIF":4.1000,"publicationDate":"2025-08-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Plant Science","FirstCategoryId":"99","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0168945225003486","RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}
引用次数: 0

Abstract

Phytophthora infestans, a destructive hemibiotrophic pathogen, relies on effector proteins to modulate host immunity and facilitate infection. However, the molecular mechanisms by which these effectors suppress host cell death during the biotrophic phase remain poorly understood. In this study, we identified three RXLR effectors—designated as Cell Death Suppressors (CDS1: Pi02860, CDS2: Pi04089, and CDS5: Pi06099)—that strongly suppress effector-triggered cell death in Nicotiana benthamiana. These CDSs are highly expressed during the early biotrophic phase and inhibit cell death triggered by diverse elicitors, including INF1, NPP1.1, Rpiblb2/Avrblb2, and Avr3a/R3a. Subcellular localization analysis revealed that the nuclear targeting is essential for their cell death suppressive activity. Functional assays demonstrated that CDS1 significantly enhances P. infestans virulence, while CDS2 and CDS5 contribute synergistically when co-expressed. Moreover, homologs of CDS1 from other Phytophthora species exhibited similar suppressive activity, despite lacking obvious sequence or structural features predictive of function. Our findings suggest that P. infestans utilizes a coordinated set of nuclear-targeting effectors to suppress host immunity during early colonization, offering new insights into pathogen strategies for immune evasion.
疫霉菌RXLR效应物抑制宿主细胞死亡并通过本菌烟草的核定位提高毒力。
疫霉(Phytophthora infestans)是一种破坏性的半生物营养病原体,依靠效应蛋白调节宿主免疫,促进感染。然而,这些效应物在生物营养期抑制宿主细胞死亡的分子机制仍然知之甚少。在这项研究中,我们确定了三种RXLR效应物,它们被指定为细胞死亡抑制因子(CDS1: Pi02860, CDS2: Pi04089和CDS5: Pi06099),它们强烈抑制效应物引发的benthamiana细胞死亡。这些cds在早期生物营养阶段高度表达,并抑制多种激发子触发的细胞死亡,包括INF1、NPP1.1、Rpiblb2/Avrblb2和Avr3a/R3a。亚细胞定位分析表明,核靶向对其细胞死亡抑制活性至关重要。功能分析表明,CDS1显著增强了P. infestans的毒力,而CDS2和CDS5在共表达时协同作用。此外,来自其他疫霉菌物种的CDS1同源物显示出类似的抑制活性,尽管缺乏明显的序列或结构特征预测功能。我们的研究结果表明,在早期定植过程中,病原菌利用一套协调的核靶向效应物抑制宿主免疫,为病原体免疫逃避策略提供了新的见解。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
Plant Science
Plant Science 生物-生化与分子生物学
CiteScore
9.10
自引率
1.90%
发文量
322
审稿时长
33 days
期刊介绍: Plant Science will publish in the minimum of time, research manuscripts as well as commissioned reviews and commentaries recommended by its referees in all areas of experimental plant biology with emphasis in the broad areas of genomics, proteomics, biochemistry (including enzymology), physiology, cell biology, development, genetics, functional plant breeding, systems biology and the interaction of plants with the environment. Manuscripts for full consideration should be written concisely and essentially as a final report. The main criterion for publication is that the manuscript must contain original and significant insights that lead to a better understanding of fundamental plant biology. Papers centering on plant cell culture should be of interest to a wide audience and methods employed result in a substantial improvement over existing established techniques and approaches. Methods papers are welcome only when the technique(s) described is novel or provides a major advancement of established protocols.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:604180095
Book学术官方微信