Abstract
BackgroundPseudomonas syringae pv. tabaci (Pstab) is the causal agent of wildfire disease in tobacco plants. Several pathovars of Pseudomonas syringae produce a phytotoxic extracellular metabolite called coronatine (COR). COR has been shown to suppress plant defense responses. Interestingly, Pstab does not produce COR but still actively suppresses early plant defense responses. It is not clear if Pstab produces any extracellular metabolites that actively suppress early defense during bacterial pathogenesis.ResultsWe found that the Pstab extracellular metabolite extracts (Pstab extracts) remarkably suppressed stomatal closure and nonhost hypersensitive response (HR) cell death induced by a nonhost pathogen, P. syringae pv. tomato T1 (Pst T1), in Nicotiana benthamiana. We also found that the accumulation of nonhost pathogens, Pst T1 and P. syringae pv. glycinea (Psgly), was increased in N. benthamiana plants upon treatment with Pstab extracts . The HR cell death induced by Pathogen-Associated Molecular Pattern (INF1), gene-for-gene interaction (Pto/AvrPto and Cf-9/AvrCf-9) and ethanol was not delayed or suppressed by Pstab extracts. We performed metabolite profiling to investigate the extracellular metabolites from Pstab using UPLC-qTOF-MS and identified 49 extracellular metabolites from the Pstab supernatant culture. The results from gene expression profiling of PR-1, PR-2, PR-5, PDF1.2, ABA1, COI1, and HSR203J suggest that Pstab extracellular metabolites may interfere with SA-mediated defense pathways.ConclusionsIn this study, we found that Pstab extracts suppress plant defense responses such as stomatal closure and nonhost HR cell death induced by the nonhost bacterial pathogen Pst T1 in N. benthamiana.
Highlights
Pseudomonas syringae pv. tabaci (Pstab) is the causal agent of wildfire disease in tobacco plants
Only a few fluorescent spots were detected on N. benthamiana leaves infected with pv. tomato strain T1 (Pst T1) and on tomato plants infected with Pstab (Figure 1A)
We speculate that the nonhost hypersensitive response (HR) cell death in N. benthamiana is triggered either by pathogen-associated molecular patterns (PAMPs) or effectors of the nonhost pathogen, Pst T1
Summary
Pseudomonas syringae pv. tabaci (Pstab) is the causal agent of wildfire disease in tobacco plants. Pstab does not produce COR but still actively suppresses early plant defense responses. It is not clear if Pstab produces any extracellular metabolites that actively suppress early defense during bacterial pathogenesis Foliar bacterial phytopathogens such as the Pseudomonas syringae species survive on the plant leaf surface as epiphytes [1]. During the initial infection process, the bacterial pathogens produce virulence factors including effector proteins and secondary metabolites, to inactivate early plant defense responses such as stomata-based immunity [2,3] and hypersensitive response (HR) cell death at the site of infection [4]. Certain bacterial pathogens have evolved to deliver specific virulence factors such as coronatine (COR) to overcome PAMP-triggered immunity (PTI) and stomata-based defense
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