Rufián José S, Lucía Ainhoa, Rueda-Blanco Javier, Zumaquero Adela, Guevara Carlos M, Ortiz-Martín Inmaculada, Ruiz-Aldea Gonzalo, Macho Alberto P, Beuzón Carmen R, Ruiz-Albert Javier
Departamento Biología Celular, Genética y Fisiología, Instituto de Hortofruticultura Subtropical y Mediterránea, Universidad de Málaga-Consejo Superior de Investigaciones Científicas, Málaga, Spain.
Shanghai Center for Plant Stress Biology, CAS Center for Excellence in Molecular Plant Sciences, Shanghai Institutes of Biological Sciences, Chinese Academy of Sciences, Shanghai, China.
Front Plant Sci. 2018 Aug 14;9:977. doi: 10.3389/fpls.2018.00977. eCollection 2018.
Many type III-secreted effectors suppress plant defenses, but can also activate effector-triggered immunity (ETI) in resistant backgrounds. ETI suppression has been shown for a number of type III effectors (T3Es) and ETI-suppressing effectors are considered part of the arms race model for the co-evolution of bacterial virulence and plant defense. However, ETI suppression activities have been shown mostly between effectors not being naturally expressed within the same strain. Furthermore, evolution of effector families is rarely explained taking into account that selective pressure against ETI-triggering effectors may be compensated by ETI-suppressing effector(s) translocated by the same strain. The HopZ effector family is one of the most diverse, displaying a high rate of loss and gain of alleles, which reflects opposing selective pressures. HopZ effectors trigger defense responses in a variety of crops and some have been shown to suppress different plant defenses. Mutational changes in the sequence of ETI-triggering effectors have been proposed to result in the avoidance of detection by their respective hosts, in a process called pathoadaptation. We analyze how deleting or overexpressing HopZ1a and HopZ3 affects virulence of HopZ-encoding and non-encoding strains. We find that both effectors trigger immunity in their plant hosts only when delivered from heterologous strains, while immunity is suppressed when delivered from their native strains. We carried out screens aimed at identifying the determinant(s) suppressing HopZ1a-triggered and HopZ3-triggered immunity within their native strains, and identified several effectors displaying suppression of HopZ3-triggered immunity. We propose effector-mediated cross-suppression of ETI as an additional force driving evolution of the HopZ family.
许多III型分泌效应蛋白可抑制植物防御，但在抗性背景下也能激活效应蛋白触发的免疫反应（ETI）。多种III型效应蛋白（T3Es）已被证明具有ETI抑制作用，并且ETI抑制效应蛋白被认为是细菌毒力与植物防御共同进化的军备竞赛模型的一部分。然而，ETI抑制活性大多表现在同一菌株中未自然表达的效应蛋白之间。此外，在考虑到针对ETI触发效应蛋白的选择压力可能由同一菌株分泌的ETI抑制效应蛋白来补偿的情况下，效应蛋白家族的进化很少得到解释。HopZ效应蛋白家族是最多样化的家族之一，显示出高频率的等位基因丢失和获得，这反映了相反的选择压力。HopZ效应蛋白在多种作物中触发防御反应，并且一些已被证明可抑制不同的植物防御。有人提出，ETI触发效应蛋白序列中的突变会导致其各自宿主无法检测到它们，这一过程称为致病适应。我们分析了缺失或过表达HopZ1a和HopZ3如何影响编码HopZ和不编码HopZ的菌株的毒力。我们发现，只有当这两种效应蛋白从异源菌株传递时，它们才会在植物宿主中触发免疫反应，而当从其天然菌株传递时，免疫反应会受到抑制。我们进行了筛选，旨在鉴定在其天然菌株中抑制HopZ1a触发和HopZ3触发免疫反应的决定因素，并鉴定出了几种显示出对HopZ3触发免疫反应有抑制作用的效应蛋白。我们提出，效应蛋白介导的ETI交叉抑制是驱动HopZ家族进化的另一种力量。
