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来自辣椒疫霉的XopAE效应蛋白靶向HSP20样p23共伴侣蛋白以抑制植物基础免疫。

The XopAE Effector from pv. Targets HSP20-like p23 Cochaperone to Suppress Plant Basal Immunity.

作者信息

Gómez De La Cruz Diana, Castillo Darwin A, Trujillo B César A, Medina Cesar A, Hurtado-McCormick Valentina, Gil Juliana, Padmanabhan Meenu, Restrepo Silvia, Dinesh-Kumar Savithramma P, Germain Hugo, López Camilo, Bernal Adriana

机构信息

Laboratory of Molecular Interactions of Agricultural Microbes, LIMMA, Department of Biological Sciences, Universidad de los Andes, Bogotá, Colombia.

Laboratory of Mycology and Plant Pathology Uniandes, Department of Biological Sciences, Universidad de los Andes, Bogotá, Colombia.

出版信息

Mol Plant Microbe Interact. 2025 May;38(3):365-375. doi: 10.1094/MPMI-08-24-0086-R. Epub 2025 Jun 5.

DOI:10.1094/MPMI-08-24-0086-R
PMID:39836062
Abstract

Pathogenic bacteria use Type 3 effector proteins to manipulate host defenses and alter metabolism to favor their survival and spread. The non-model bacterial pathogen pv. () causes devastating disease in cassava. The molecular role of Type 3 effector proteins from in causing disease is largely unknown. Here, we report that the XopAE effector from suppresses plant defense responses. Our results show that XopAE is a suppressor of basal defenses such as callose deposition and the production of reactive oxygen species. XopAE targets a small heat shock protein (p23-1 cochaperone) in cassava and its homolog p23-1 in . XopAE localizes to the nucleus and in scattered points throughout the cell border, whereas p23-1 shows a nucleocytoplasmic localization. Upon interaction, XopAE hijacks p23-1 to the scattered points throughout the cell border, and they also interact in the nucleus. Our results indicate that the interaction between XopAE and p23-1 is essential for suppressing basal plant defense. This study is one of the first to address the molecular mechanisms deployed by to cause disease in cassava, a non-model crop plant. [Formula: see text] Copyright © 2025 The Author(s). This is an open access article distributed under the CC BY-NC-ND 4.0 International license.

摘要

致病细菌利用III型效应蛋白来操纵宿主防御并改变新陈代谢,以利于它们的存活和传播。非模式细菌病原体木薯细菌性枯萎病菌(Xanthomonas axonopodis pv. manihotis)会在木薯中引发毁灭性疾病。来自木薯细菌性枯萎病菌的III型效应蛋白在致病过程中的分子作用很大程度上尚不清楚。在此,我们报道木薯细菌性枯萎病菌的XopAE效应蛋白可抑制植物防御反应。我们的结果表明,XopAE是胼胝质沉积和活性氧产生等基础防御的抑制因子。XopAE靶向木薯中的一种小热激蛋白(p23-1共伴侣蛋白)及其在烟草中的同源物p23-1。XopAE定位于细胞核以及整个细胞边界的分散点,而p23-1表现出核质定位。相互作用时,XopAE将p23-1劫持到整个细胞边界的分散点,并且它们在细胞核中也相互作用。我们的结果表明,XopAE与p23-1之间的相互作用对于抑制植物基础防御至关重要。本研究是首批探讨木薯细菌性枯萎病菌在非模式作物木薯中致病所采用分子机制的研究之一。[公式:见正文] 版权所有© 2025作者。本文是一篇根据知识共享署名-非商业性使用-禁止演绎4.0国际许可协议分发的开放获取文章。

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