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Background   Pseudomonas 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.    Results  We 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.    Conclusions  In 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 .

Suppression of plant defense responses by extracellular metabolites from Pseudomonas syringae pv. tabaci in Nicotiana benthamiana