HYR1-mediated detoxification of reactive oxygen species is required for full virulence in the rice blast fungus.

HYR1-mediated detoxification of reactive oxygen species is required for full virulence in the rice blast fungus.
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DOI:
10.1371/journal.ppat.1001335
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发表时间:
2011-04
期刊:
影响因子:
6.7
通讯作者:
Donofrio NM
Donofrio NM
中科院分区:
医学1区
文献类型:
--
作者:
Huang K;Czymmek KJ;Caplan JL;Sweigard JA;Donofrio NM

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在植物与病原体相互作用的过程中,植物可能会产生几种类型的防御反应,要么完全阻断病原体,要么减轻疾病的数量。这些反应包括释放活性氧(ROS)来攻击病原体,以及形成细胞壁附着(CWAs)来物理阻止病原体的渗透。一个成功的病原体可能有自己的活性氧解毒机制来应对这种不适宜的环境。在这里,我们报道了稻瘟病菌(Magnaporthe oryzae)中的一种这样的候选机制,它由一个我们称之为MoHYR1的基因控制。该基因(MGG_07460)编码谷胱甘肽过氧化物酶(GSHPx)结构域,据报道其在酵母中的同源物特异性解毒磷脂过氧化物。为了在m.o ryzae中表征该基因,我们产生了一个缺失mutantΔhyr1,该缺失随着过氧化氢(H2O2)的增加而显示出生长抑制。此外,我们观察到真菌突变体耐受由易感植物产生的ROS的能力下降,包括与CWAs相关的ROS。最终,这导致大麦和水稻的病变大小明显减小。为了确定该基因如何与M. oryzae中其他(ROS)清除相关基因相互作用,我们比较了突变型和野生型中10个基因在H2O2和无H2O2条件下的表达水平。我们的研究结果表明,HYR1基因对于真菌在离体和植物中耐受H2O2具有重要作用,并且这种能力与真菌毒力直接相关。活性氧(Reactive oxygen species, ROS)是一种抗菌化合物,也是植物防御反应的刺激物和产物。活性氧似乎在病原体和植物接触的关键区域活跃。因此,了解ROS在每个相互作用伙伴中的来源、作用和目的地对于理解病原体-宿主分子战至关重要。在这项研究中,我们重点研究了一种潜在的真菌机制,可以在感染的早期阶段改善植物产生的ROS的作用。从稻瘟病菌Magnaporthe oryzae中提取的MoHYR1基因的鉴定表明,MoHYR1参与克服植物防御产生的ROS。该基因的缺失导致m.o ryzae的毒力缺陷,我们认为这与突变体无法解毒植物产生的ROS有关。总之,我们的数据表明,HYR1是稻瘟病病原体的一个毒力因子,它在毒力中的作用与早期感染事件中植物产生的ROS的感知和管理直接相关。HYR1是酵母中活性氧清除和感知途径的一部分,我们的研究首次在丝状真菌中检测了这一重要基因。
During plant-pathogen interactions, the plant may mount several types of defense responses to either block the pathogen completely or ameliorate the amount of disease. Such responses include release of reactive oxygen species (ROS) to attack the pathogen, as well as formation of cell wall appositions (CWAs) to physically block pathogen penetration. A successful pathogen will likely have its own ROS detoxification mechanisms to cope with this inhospitable environment. Here, we report one such candidate mechanism in the rice blast fungus, Magnaporthe oryzae, governed by a gene we refer to as MoHYR1. This gene (MGG_07460) encodes a glutathione peroxidase (GSHPx) domain, and its homologue in yeast was reported to specifically detoxify phospholipid peroxides. To characterize this gene in M. oryzae, we generated a deletion mutantΔhyr1 which showed growth inhibition with increased amounts of hydrogen peroxide (H2O2). Moreover, we observed that the fungal mutants had a decreased ability to tolerate ROS generated by a susceptible plant, including ROS found associated with CWAs. Ultimately, this resulted in significantly smaller lesion sizes on both barley and rice. In order to determine how this gene interacts with other (ROS) scavenging-related genes in M. oryzae, we compared expression levels of ten genes in mutant versus wild type with and without H2O2. Our results indicated that the HYR1 gene was important for allowing the fungus to tolerate H2O2 in vitro and in planta and that this ability was directly related to fungal virulence. Reactive oxygen species (ROS) are antimicrobial compounds and also serve as stimulators and products of plant defense reactions. ROS appear to be active in the critical zone where pathogens and plants come in contact. Therefore, understanding the source, the role, and the destination of ROS in each interacting partner will be crucial for understanding the pathogen-host molecular battle. In this study, we focused on one potential fungal mechanism for ameliorating effects of plant-produced ROS during the early stages of infection. Characterizing the MoHYR1 gene from the rice blast fungus Magnaporthe oryzae, suggested that MoHYR1 was involved in overcoming plant defense-generated ROS. The deletion of this gene caused a virulence defect in M. oryzae, which we believe was associated with the mutant's inability to detoxify plant-generated ROS. Together, our data suggested that HYR1 is a virulence factor in the rice blast pathogen, and its role in virulence was directly related to sensing and managing plant-generated ROS during early infection events. HYR1 is part of a ROS scavenging and sensing pathway that is well characterized in yeast, and our study is the first to examine this important gene in filamentous fungi.
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