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Thiamine confers systemic acquired resistance (SAR) on susceptible plants through priming, leading to rapid counterattack against pathogen invasion and perturbation of disease progress. Priming reduces the metabolic cost required for constitutive expression of acquired resistance. To investigate the effects of priming by thiamine on defense-related responses, Arabidopsis (Arabidopsis thaliana) was treated with thiamine and effects of pathogen challenge on the production of active oxygen species, callose deposition, hypersensitive cell death, and pathogenesis-related 1 (PR1)/Phe ammonia-lyase 1 (PAL1) gene expression was analyzed. Thiamine did not induce cellular and molecular defense responses except for transient expression of PR1 per se; however, subsequent Pseudomonas syringae pv tomato challenge triggered pronounced cellular defense responses and advanced activation of PR1/PAL1 gene transcription. Thiamine treatment and subsequent pathogen invasion triggered hydrogen peroxide accumulation, callose induction, and PR1/PAL1 transcription activation in Arabidopsis mutants insensitive to jasmonic acid (jar1), ethylene (etr1), or abscisic acid (abi3-3), but not in plants expressing bacterial NahG and lacking regulation of SAR (npr1 [nonexpressor of PR genes 1]). Moreover, removal of hydrogen peroxide by catalase almost completely nullified cellular and molecular defense responses as well as SAR abolishing bacterial propagation within plants. Our results indicated that priming is an important cellular mechanism in SAR by thiamine and requires hydrogen peroxide and intact NPR1.
Plants have developed an effective immanent surveillance mechanism and pathogen invasions often induce ubiquitous plant defense responses that activate biochemical and structural changes within plant cells. A specific plant's resistance (R) gene product functions as a signaling receptor for the corresponding avirulence (Avr) gene product from the pathogen. The key differences between the compatible (susceptible) and incompatible (resistant) interactions are the early recognition of pathogen attack and the timely expression of defense responses (Yang et al., 1997; McDowell and Dangl, 2000; Lu et al., 2004; Bennett et al., 2005). One of the most noticeable features in the incompatible interaction is abrupt cell death, also termed hypersensitive response (HR), a restricted cell death defining further pathogen progress, which is initiated by the interaction between the R gene product and the Avr gene product. R gene-dependent resistance has been known to share several defense-related responses with systemic resistance induced by plant defense activators.
Systemic resistance is induced by exogenous application of salicylic acid (SA; Delaney,...