Bacillus amyloliquefaciens PMB05 Increases Resistance to Bacterial Wilt by Activating Mitogen-Activated Protein Kinase and Reactive Oxygen Species Pathway Crosstalk in Arabidopsis thaliana.

Bacterial wilt caused by Ralstonia solanacearum 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 Bacillus amyloliquefaciens PMB05 can control bacterial wilt through intensifying immune signals triggered by a pathogen-associated molecular pattern (PAMP) from R. solanacearum. 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 wrky22 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 mekk1, mkk5, and mpk6 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 rbohD 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.

Bacillus amyloliquefaciens Strain PMB05 Intensifies Plant Immune Responses to Confer Resistance Against Bacterial Wilt of Tomato.

Tomato is an economic crop worldwide. Many limiting factors reduce the production of tomato, with bacterial wilt caused by Ralstonia solanacearum being the most destructive disease. Our previous study showed that the disease resistance to bacterial soft rot is enhanced by Bacillus amyloliquefaciens strain PMB05. This enhanced resistance is associated with the intensification of pathogen-associated molecular patterns (PAMP)-triggered immunity (PTI). To determine whether the PTI-intensifying Bacillus spp. strains are able to confer disease resistance to bacterial wilt, their effects on PTI signals triggered by PAMP from R. solanacearum and on the occurrence of bacterial wilt were assayed. Before assay, a gene that encodes harpin from R. solanacearum, PopW, was applied as a PAMP. Results revealed that the B. amyloliquefaciens strain PMB05 was the one strain among 9 Bacillus rhizobacterial strains which could significantly intensify the PopW-induced hypersensitive response (HR) on Arabidopsis leaves. Moreover, we observed that the signals of PopW-induced reactive oxygen species generation and callose deposition were increased, confirming that the PTI was intensified by PMB05. The intensification of the PopW-triggered HR by PMB05 in Arabidopsis was reduced upon treatment with inhibitors in PTI pathways. Furthermore, the application of Bacillus spp. strains on tomato plants showed that only the use of PMB05 resulted in significantly increased resistance to bacterial wilt. Moreover, the PTI signals were also intensified in the tomato leaves. Taken together, we demonstrated that PMB05 is a PTI-intensifying bacterium that confers resistance to tomato bacterial wilt. Screening of plant immunity intensifying rhizobacteria is a possible strategy to control tomato bacterial wilt.[Formula: see text] Copyright © 2020 The Author(s). This is an open access article distributed under the CC BY-NC-ND 4.0 International license.