Teper Doron, Xu Jin, Pandey Sheo Shankar, Wang Nian
Citrus Research and Education Center, Department of Microbiology and Cell Science, Institute of Food and Agricultural Sciences, University of Florida, 700 Experiment Station Road, Lake Alfred, FL 33850, U.S.A.
Mol Plant Microbe Interact. 2021 Sep;34(9):1033-1047. doi: 10.1094/MPMI-01-21-0026-R. Epub 2021 Oct 7.
Citrus canker disease caused by subsp. is one of the most destructive diseases in citrus. subsp. pathotypes display different host ranges. subsp. strain A () causes canker disease in most commercial citrus varieties, whereas strain AW (), which is genetically similar to , infects only lime and alemow. Understanding the mechanism that determines the host range of pathogens is critical to investigating and utilizing host resistance. We hypothesized that would undergo mutations in genes that restrict its host range when artificially inoculated into incompatible citrus varieties. To test this hypothesis, we used an experimental evolution approach to identify phenotypic traits and genetic loci associated with the adaptation of to incompatible sweet orange. Repeated inoculation and reisolation cycles improved the ability of three independent strains to colonize sweet orange. Adapted strains displayed increased expression of type III secretion system and effector genes. Genome sequencing analysis indicated that two of the adapted strains harbored mutations in , a transcription activator-like effector (TALE) gene, that corresponded to the removal of one or two repeats from the central DNA-binding repeat region. Introduction of the original but not the adapted variants into abolished its ability to cause canker symptoms in sweet orange, Meyer lemon, and clementine but not in other -resistant citrus varieties. The original , when expressed in , induced ion leakage and the expression of pathogenesis-related genes but had no effect on expression in sweet orange. Our study has identified a novel host-specific avirulence TALE and demonstrated active adaptive rearrangements of the TALE repeat array during host adaptation.[Formula: see text] Copyright © 2021 The Author(s). This is an open access article distributed under the CC BY-NC-ND 4.0 International license.
由 亚种引起的柑橘溃疡病是柑橘中最具毁灭性的病害之一。 亚种致病型表现出不同的寄主范围。 亚种A菌株（ ）在大多数商业柑橘品种中引起溃疡病，而与 基因相似的AW菌株（ ）仅感染酸橙和阿蕾檬。了解决定病原体寄主范围的机制对于研究和利用寄主抗性至关重要。我们假设，当 被人工接种到不相容的柑橘品种中时，其限制寄主范围的基因会发生突变。为了验证这一假设，我们采用实验进化方法来鉴定与 适应不相容甜橙相关的表型特征和基因位点。重复接种和再分离循环提高了三个独立的 菌株在甜橙上定殖的能力。适应后的 菌株III型分泌系统和效应子基因的表达增加。基因组测序分析表明，两个适应后的菌株在一个类转录激活因子效应子（TALE）基因 中发生了突变，这对应于中央DNA结合重复区域中一个或两个重复序列的缺失。将原始的而非适应后的 变体导入 后，它在甜橙、 Meyer柠檬和克莱门氏小柑橘中导致溃疡症状的能力丧失，但在其他抗 的柑橘品种中则没有影响。原始的 在 中表达时，会诱导离子渗漏和病程相关基因的表达，但对甜橙中的 表达没有影响。我们的研究鉴定出一种新的寄主特异性无毒TALE，并证明了在寄主适应过程中TALE重复阵列的活跃适应性重排。[公式：见正文] 版权所有© 2021作者。这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。
