Li Ai-Ting, Liu Shang-Kai, Li Jia-Rong, Blanco Sabrina Diana, Tsai Hsin-Wei, Xie Jia-Xin, Tsai Yun-Chen, Tzean Yuh, Lin Yi-Hsien
Department of Plant Medicine, National Pingtung University of Science and Technology, Pingtung 912301, Taiwan.
Department of Tropical Agriculture and International Cooperation, National Pingtung University of Science and Technology, Pingtung 912301, Taiwan.
Plants (Basel). 2024 Sep 16;13(18):2591. doi: 10.3390/plants13182591.
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 PMB05 can enhance PTI signals and improve disease control of bacterial soft rot and wilt in . 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 PMB05 in controlling bacterial soft rot. In this study, ecotype Columbia (Col-0) and its mutants on a MAPK pathway-related pathway were used as a model and established that the ability of 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 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.
当植物受到病原体感染时，会启动内源性免疫反应。当这些防御反应的启动由病原体的病原体相关分子模式（PAMP）诱导时，称为PAMP触发的免疫（PTI）。先前的研究表明，PMB05可以增强PTI信号，并改善对细菌性软腐病和枯萎病的病害控制。在控制青枯病的背景下，丝裂原活化蛋白激酶（MAPK）信号通路的参与已得到证实。然而，该通路在PMB05控制细菌性软腐病中是否也有必要尚不清楚。在本研究中，以生态型哥伦比亚（Col-0）及其在MAPK通路相关途径上的突变体为模型，证实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，而不是与胼胝质沉积相关。采用喷雾接种法表明，PMB05可以增强气孔关闭，从而限制软腐病菌的入侵。这种控制机制也已被证明需要MAPK通路的激活。本研究表明，PMB05可以在PTI期间通过激活MAPK通路加速气孔关闭，从而减少病原体入侵并实现对细菌性软腐病的抗病性。
