Ralstonia solanacearum Encounters an Oxidative Environment During Tomato Infection

Ralstonia solanacearum Encounters an Oxidative Environment During Tomato Infection
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DOI:
10.1094/mpmi-22-7-0773
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发表时间:
2009-07-01
影响因子:
3.5
通讯作者:
Allen, Caitilyn
Allen, Caitilyn
中科院分区:
生物学2区
文献类型:
--
作者:
Flores-Cruz, Zomary;Allen, Caitilyn

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番茄感染过程中诱导的青枯雷尔斯顿氏菌基因表明,这种病原体在青枯病发病过程中会遇到活性氧(ROS)。青枯菌的基因组含有多种多余的 ROS 清除酶,间接证据表明该病原体在其生命周期中经历了强烈的氧化应激。超过 9% 的细菌植物诱导基因也被培养物中的过氧化氢上调,这表明氧化应激可能与植物宿主的生命有关。被青枯菌感染的番茄叶子含有过氧化氢,并且这种活性氧的浓度随着病原体数量的增加而增加。植物诱导的预测过氧化物酶基因 bcp 的诱变导致青枯菌菌株在培养物中解毒 ROS 的能力降低。 bcp突变体导致番茄青枯病的发病略有延迟。此外,它的毒力在经过改造以过量产生过氧化氢的烟草植物上显着降低,这表明 Bcp 对于植物来源的过氧化氢的解毒是必需的,并提供了宿主 ROS 可以限制这种病原体成功的证据。这些结果表明,青枯菌在发病过程中暴露于ROS,并进化出冗余且有效的氧化应激反应来适应宿主环境并引起疾病。
Ralstonia solanacearum genes that are induced during tomato infection suggested that this pathogen encounters reactive oxygen species (ROS) during bacterial wilt pathogenesis. The genomes of R. solanacearum contain multiple redundant ROS-scavenging enzymes, indirect evidence that this pathogen experiences intense oxidative stress during its life cycle. Over 9% of the bacterium's plant-induced genes were also upregulated by hydrogen peroxide in culture, suggesting that oxidative stress may be linked to life in the plant host. Tomato leaves infected by R. solanacearum contained hydrogen peroxide, and concentrations of this ROS increased as pathogen populations increased. Mutagenesis of a plant-induced predicted peroxidase gene, bcp, resulted in an R. solanacearum strain with reduced ability to detoxify ROS in culture. The bcp mutant caused slightly delayed bacterial wilt disease onset in tomato. Moreover, its virulence was significantly reduced on tobacco plants engineered to overproduce hydrogen peroxide, demonstrating that Bcp is necessary for detoxification of plant-derived hydrogen peroxide and providing evidence that host ROS can limit the success of this pathogen. These results reveal that R. solanacearum is exposed to ROS during pathogenesis and that it has evolved a redundant and efficient oxidative stress response to adapt to the host environment and cause disease.