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.

Bacterial soft rot, caused by Pectobacterium carotovorum subsp. carotovorum, affects numerous vegetable crops. Beneficial microbes like Bacillus amyloliquefaciens PMB05 offer a sustainable alternative to traditional copper- or antibiotic-based controls, which risks the development of pathogen resistance. Bacillus amyloliquefaciens PMB05 enhances disease resistance to soft rot by intensifying PAMP-triggered immunity (PTI). Although our previous research showed that PMB05-intensified PTI correlates with a reduced photosynthetic electron transport rate under high light conditions, it remains unclear whether increasing light intensity can strengthen PMB05-mediated immune signaling to further enhance disease resistance in plant leaves. In this study, Arabidopsis plants were grown under varying light intensities to address this question. Furthermore, expression of the type III elicitor, HrpN protein, was applied to evaluate the impact of PMB05 treatment on immune activation. HrpN acts as a PAMP that can trigger plant defense responses. The results revealed that higher growth light intensity was associated with PMB05-intensified PTI response by increasing reactive oxygen species generation but suppresses callose deposition. In addition, PMB05-facilitated PTI-mediated stomatal closure occurred more rapidly and tightly under high light, thereby restricting pathogen invasion into leaf tissues. Disease assays further confirmed that higher light intensity significantly reduced soft rot severity in A. thaliana, while the combination of high light and PMB05 treatment achieved superior control efficacy. Furthermore, PMB05-associated disease protection under high growth light was not detected in sid2, npr1, and nahG plants, indicating that intact SA-associated functions are required for the detectable protective phenotype under the conditions tested. These findings demonstrate that environmental light management can strategically potentiate immunity-intensifying microbes, establishing a novel paradigm for sustainable disease control through the coordinated manipulation of light conditions and microbial application.