Chuang Chiao-Yu, Lin Si-Ting, Li Ai-Ting, Li Sin-Hua, Hsiao Chia-Yu, Lin Yi-Hsien
Department of Plant Medicine, National Pingtung University of Science and Technology, Pingtung, Taiwan.
Phytopathology. 2022 Dec;112(12):2495-2502. doi: 10.1094/PHYTO-04-22-0134-R. Epub 2022 Dec 20.
Bacterial wilt caused by can infect many crops, causing significant losses worldwide. The use of beneficial microorganisms is considered a feasible method for controlling this disease. Our previous study showed that PMB05 can control bacterial wilt through intensifying immune signals triggered by a pathogen-associated molecular pattern (PAMP) from . It is still uncertain whether induction of the mitogen-activated protein kinase (MAPK) pathway during PAMP-triggered immunity (PTI) is responsible for enhancing disease resistance. To gain more insights on how the presence of PMB05 regulates PTI signaling, its association with the MAPK pathway was assayed. Our results showed that the activation of MPK3/6 and expression of upon treatment with the PAMP, PopW, was increased during co-treatment with PMB05. Moreover, the disease resistance conferred by PMB05 to bacterial wilt was abolished in , , and mutants. To determine the relationship between the MAPK pathway and plant immune signals, the assay on reactive oxygen species (ROS) generation and callose deposition showed that only the ROS generation was strongly reduced in these mutants. Because ROS generation is highly correlated with RbohD, the results revealed that the effects of PMB05 on both PopW-induced ROS generation and disease resistance to bacterial wilt were eliminated in the mutant, suggesting that the generation of ROS is also required for PMB05-enhanced disease resistance. Taken together, we concluded that the crosstalk between the initiation of ROS generation and further activation of the MAPK pathway is necessary when PMB05 is used to improve disease resistance to bacterial wilt. [Formula: see text] Copyright © 2022 The Author(s). This is an open access article distributed under the CC BY-NC-ND 4.0 International license.
由[病原体名称未给出]引起的青枯病可感染多种作物,在全球范围内造成重大损失。使用有益微生物被认为是控制这种疾病的一种可行方法。我们之前的研究表明,PMB05可通过增强由[病原体名称未给出]的病原体相关分子模式(PAMP)触发的免疫信号来控制青枯病。在PAMP触发的免疫(PTI)过程中,丝裂原活化蛋白激酶(MAPK)途径的诱导是否负责增强抗病性仍不确定。为了更深入了解PMB05的存在如何调节PTI信号传导,我们检测了它与MAPK途径的关联。我们的结果表明,在用PAMP PopW处理时,与PMB05共同处理期间MPK3/6的激活和[基因名称未给出]的表达增加。此外,在[基因名称未给出]、[基因名称未给出]和[基因名称未给出]突变体中,PMB05赋予的对青枯病的抗病性被消除。为了确定MAPK途径与植物免疫信号之间的关系,对活性氧(ROS)产生和胼胝质沉积的检测表明,在这些突变体中只有ROS产生强烈减少。因为ROS产生与RbohD高度相关,结果表明在[基因名称未给出]突变体中,PMB05对PopW诱导的ROS产生和对青枯病的抗病性的影响都被消除了,这表明ROS的产生对于PMB05增强的抗病性也是必需的。综上所述,我们得出结论,当使用PMB05提高对青枯病的抗病性时,ROS产生的起始与MAPK途径的进一步激活之间的相互作用是必要的。[公式:见正文] 版权所有© 2022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。