Quercetin-induced H(2)O(2) mediates the pathogen resistance against Pseudomonas syringae pv. Tomato DC3000 in Arabidopsis thaliana.

Quercetin is a potent antioxidant and has been extensively used as a therapy intervention to prevent age-associated diseases. However, emerging studies showed it can also act as a prooxidant and induce H(2)O(2) under certain conditions. In the current study, our results showed that quercetin contributed to the pathogen resistance in Arabidopsis thaliana (Arabidopsis) in response to the infection of virulent strain Pseudomonas syringae pv. Tomato DC3000 (Pst). Various defense responses, such as H(2)O(2) burst, callose deposition, cell death, PR1 (pathogenesis-related 1) and PAL1 (Phe ammonia-lyase 1) gene expression, have been investigated in quercetin-pretreated Pst-inoculated Arabidopsis Col-0 and there was a strong defensive response in quercetin-pretreated Arabidopsis against virulent Pst. However, with the presence of catalase, the protective effects of quercetin on pathogen resistance to virulent Pst disappeared in Arabidopsis, suggesting that H(2)O(2) may play a key role in plant defense responses. In addition, we confirmed that quercetin did not show any beneficial effect on pathogen-free leaves in Arabidopsis, indicating that pathogen challenge is also required to induce the defense responses in quercetin-pretreated Arabidopsis. Furthermore, strong defense responses have been observed in quercetin-pretreated Arabidopsis mutant jar1, ein2, and abi1-2 under Pst challenge, whereas no protective effect has been observed in quercetin-pretreated Arabidopsis mutant NahG and npr1. These findings indicate that quercetin induces the resistance to Pst in Arabidopsis via H(2)O(2) burst and involvement of SA and NPR1.

AtMYB44 positively modulates disease resistance to Pseudomonas syringae through the salicylic acid signalling pathway in Arabidopsis.

Plant MYB transcription factors are implicated in resistance to biotic and abiotic stresses. Here, we demonstrate that an R2-R3 MYB transcription factor, AtMYB44, plays a role in the plant defence response to the bacterial pathogen Pseudomonas syringae pv. tomato DC3000 (PstDC3000). The expression of AtMYB44 was upregulated upon pathogen infection and treatments with defence-related phytohormones. Transgenic plants overexpressing AtMYB44 (35S-Ms) exhibited greater levels of PR1 gene expression, cell death, callose deposition and hydrogen peroxide (H2O2) accumulation in leaves infected with PstDC3000. Consequently, 35S-M lines displayed enhanced resistance to PstDC3000. In contrast, the atmyb44 T-DNA insertion mutant was more susceptible to PstDC3000 and exhibited decreased PR1 gene expression upon infection. Using double mutants constructed via crosses of 35S-M lines with NahG transgenic plants and nonexpressor of pathogenesis-related genes1 mutant (npr1-1), we demonstrated that the enhanced PR1 gene expression and PstDC3000 resistance in 35S-M plants occur mainly through the salicylic acid signalling pathway.