A Mitogen-Activated Protein Kinase Pathway is Required for Bacillus amyloliquefaciens PMB05 to Enhance Disease Resistance to Bacterial Soft Rot in Arabidopsis thaliana

Plants Pub Date : 2024-09-16 DOI:10.3390/plants13182591
Ai-Ting Li, Shang-Kai Liu, Jia-Rong Li, Sabrina Diana Blanco, Hsin-Wei Tsai, Jia-Xin Xie, Yun-Chen Tsai, Yuh Tzean, Yi-Hsien Lin
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Abstract

When a plant is infected by a pathogen, endogenous immune responses are initiated. When the initiation of these defense responses is induced by a pathogen-associated molecular pattern (PAMP) of a pathogen, it is called PAMP-triggered immunity (PTI). Previous studies have shown that Bacillus amyloliquefaciens PMB05 can enhance PTI signals and improve disease control of bacterial soft rot and wilt in Arabidopsis thaliana. In the context of controlling bacterial wilt disease, the involvement of a mitogen-activated protein kinase (MAPK) signaling pathway has been established. Nevertheless, it remains unclear whether this pathway is also required for B. amyloliquefaciens PMB05 in controlling bacterial soft rot. In this study, A. thaliana ecotype Columbia (Col-0) and its mutants on a MAPK pathway-related pathway were used as a model and established that the ability of B. amyloliquefaciens PMB05 to control soft rot requires the participation of the MAPK pathway. Moreover, the enhancement of disease resistance by PMB05 is highly correlated with the activation of reactive oxygen species generation and stomata closure, rather than callose deposition. The spray inoculation method was used to illustrate that PMB05 can enhance stomatal closure, thereby restricting invasion by the soft rot bacterium. This control mechanism has also been demonstrated to require the activation of the MAPK pathway. This study demonstrates that B. amyloliquefaciens PMB05 can accelerate stomata closure via the activation of the MAPK pathway during PTI, thereby reducing pathogen invasion and achieving disease resistance against bacterial soft rot.
淀粉样芽孢杆菌 PMB05 增强拟南芥对细菌软腐病的抗病性需要一种丝裂原活化蛋白激酶途径
当植物受到病原体感染时,会启动内源免疫反应。如果这些防御反应是由病原体的病原体相关分子模式(PAMP)诱导启动的,则称为 PAMP 触发免疫(PTI)。先前的研究表明,淀粉芽孢杆菌 PMB05 可以增强 PTI 信号,改善拟南芥对细菌性软腐病和枯萎病的病害控制。在控制细菌性枯萎病的过程中,有丝分裂原激活蛋白激酶(MAPK)信号通路的参与已经得到证实。然而,目前还不清楚淀粉芽孢杆菌 PMB05 在控制细菌软腐病时是否也需要这一途径。本研究以 A. thaliana ecotype Columbia(Col-0)及其 MAPK 通路相关突变体为模型,证实 B. amyloliquefaciens PMB05 控制软腐病的能力需要 MAPK 通路的参与。此外,PMB05 对抗病性的增强与活性氧生成的激活和气孔关闭高度相关,而非胼胝质沉积。喷雾接种法说明,PMB05 能增强气孔关闭,从而限制软腐病菌的入侵。这种控制机制还被证明需要激活 MAPK 通路。本研究证明,淀粉芽孢杆菌 PMB05 可在 PTI 期间通过激活 MAPK 途径加速气孔关闭,从而减少病原体入侵,实现对细菌性软腐病的抗病性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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