Zitong Yang, Gan Ai, Xinyu Lu, Yuke Li, Jinlu Miao, Wen Song, Heng Xu, Jinding Liu, Danyu Shen, Daolong Dou
{"title":"<i>Phytophthora sojae</i> Effector PsCRN108 Targets CAMTA2 to Suppress <i>HSP40</i> Expression and ROS Burst.","authors":"Zitong Yang, Gan Ai, Xinyu Lu, Yuke Li, Jinlu Miao, Wen Song, Heng Xu, Jinding Liu, Danyu Shen, Daolong Dou","doi":"10.1094/MPMI-05-23-0058-R","DOIUrl":null,"url":null,"abstract":"<p><p>Oomycete pathogens secrete numerous crinkling and necrosis proteins (CRNs) to manipulate plant immunity and promote infection. However, the functional mechanism of CRN effectors is still poorly understood. Previous research has shown that the <i>Phytophthora sojae</i> effector PsCRN108 binds to the promoter of <i>HSP90</i>s and inhibits their expression, resulting in impaired plant immunity. In this study, we found that in addition to <i>HSP90</i>, PsCRN108 also suppressed other <i>Heat Shock Protein</i> (<i>HSP</i>) family genes, including <i>HSP40</i>. Interestingly, PsCRN108 inhibited the expression of <i>NbHSP40</i> through its promoter, but did not directly bind to its promoter. Instead, PsCRN108 interacted with NbCAMTA2, a negative regulator of plant immunity. NbCAMTA2 was a negative regulator of <i>NbHSP40</i> expression, and PsCRN108 could promote such inhibition activity of NbCAMTA2. Our results elucidated the multiple roles of PsCRN108 in the suppression of plant immunity and revealed a new mechanism by which the CRN effector hijacked transcription factors to affect immunity. [Formula: see text] Copyright © 2024 The Author(s). This is an open access article distributed under the CC BY-NC-ND 4.0 International license.</p>","PeriodicalId":3,"journal":{"name":"ACS Applied Electronic Materials","volume":null,"pages":null},"PeriodicalIF":4.3000,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"ACS Applied Electronic Materials","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1094/MPMI-05-23-0058-R","RegionNum":3,"RegionCategory":"材料科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/1/29 0:00:00","PubModel":"Epub","JCR":"Q1","JCRName":"ENGINEERING, ELECTRICAL & ELECTRONIC","Score":null,"Total":0}
引用次数: 0
Abstract
Oomycete pathogens secrete numerous crinkling and necrosis proteins (CRNs) to manipulate plant immunity and promote infection. However, the functional mechanism of CRN effectors is still poorly understood. Previous research has shown that the Phytophthora sojae effector PsCRN108 binds to the promoter of HSP90s and inhibits their expression, resulting in impaired plant immunity. In this study, we found that in addition to HSP90, PsCRN108 also suppressed other Heat Shock Protein (HSP) family genes, including HSP40. Interestingly, PsCRN108 inhibited the expression of NbHSP40 through its promoter, but did not directly bind to its promoter. Instead, PsCRN108 interacted with NbCAMTA2, a negative regulator of plant immunity. NbCAMTA2 was a negative regulator of NbHSP40 expression, and PsCRN108 could promote such inhibition activity of NbCAMTA2. Our results elucidated the multiple roles of PsCRN108 in the suppression of plant immunity and revealed a new mechanism by which the CRN effector hijacked transcription factors to affect immunity. [Formula: see text] Copyright © 2024 The Author(s). This is an open access article distributed under the CC BY-NC-ND 4.0 International license.
疫霉菌效应子PsCRN108靶向CAMTA2以抑制HSP40的表达和ROS的爆发。
卵菌病原体分泌大量的皱缩和坏死蛋白(CRNs)来操纵植物免疫并促进感染。然而,对CRN效应物的功能机制仍知之甚少。先前的研究表明,疫霉效应子PsCRN108与HSP90的启动子结合并抑制其表达,导致植物免疫受损。在这项研究中,我们发现除了HSP90,PsCRN108还抑制其他HSP家族基因,包括HSP40。有趣的是,PsCRN108通过其启动子抑制NbHSP40的表达,但不直接与其启动子结合。相反,PsCRN108与植物免疫的负调节因子NbCAMTA2相互作用。NbCAMTA2是NbHSP40表达的负调控因子,PsCRN108可促进NbCAMTA2。我们的研究结果阐明了PsCRN108在抑制植物免疫中的多种作用,并揭示了CRN效应物劫持转录因子影响免疫的新机制。
本文章由计算机程序翻译,如有差异,请以英文原文为准。