Vitamin B 1 (thiamine) is an essential nutrient for humans. Vitamin B 1 deficiency causes beriberi, which disturbs the central nervous and circulatory systems. In countries in which rice (Oryza sativa) is a major food, thiamine deficiency is prevalent because polishing of rice removes most of the thiamine in the grain. We demonstrate here that thiamine, in addition to its nutritional value, induces systemic acquired resistance (SAR) in plants. Thiamine-treated rice, Arabidopsis (Arabidopsis thaliana), and vegetable crop plants showed resistance to fungal, bacterial, and viral infections. Thiamine treatment induces the transient expression of pathogenesis-related (PR) genes in rice and other plants. In addition, thiamine treatment potentiates stronger and more rapid PR gene expression and the up-regulation of protein kinase C activity. The effects of thiamine on disease resistance and defense-related gene expression mobilize systemically throughout the plant and last for more than 15 d after treatment. Treatment of Arabidopsis ecotype Columbia-0 plants with thiamine resulted in the activation of PR-1 but not PDF1.2. Furthermore, thiamine prevented bacterial infection in Arabidopsis mutants insensitive to jasmonic acid or ethylene but not in mutants impaired in the SAR transduction pathway. These results clearly demonstrate that thiamine induces SAR in plants through the salicylic acid and Ca
21-related signaling pathways. The findings provide a novel paradigm for developing alternative strategies for the control of plant diseases.Plants, like animals, are continually exposed to pathogen attack and have developed an innate surveillance mechanism that enables them to rapidly ward off attempted invasions by pathogens. The key differences between the compatible (susceptible) and incompatible (resistant) interactions are the timely recognition of pathogen attack and the rapid, appropriate expression of defense responses (Yang et al., 1997;McDowell and Dangl, 2000;Kim et al., 2001a;Umemura et al., 2003;Lu et al., 2004;Bennett et al., 2005). In incompatible interactions, the plant's resistance (R) gene product acts as a signaling receptor for the pathogen's avirulence (Avr) gene product in the presence of resistance-regulating factors such as RAR1 and SGT1, leading to a form of cell death termed hypersensitive response (HR;Flor, 1971;Shen et al., 2003;Allen et al., 2004;Belkhadir et al., 2004;Bieri et al., 2004;Bohnert et al., 2004;Zhang et al., 2004;Rowland et al., 2005). HR-mediated cell death is triggered sequentially through an increase in the intracellular (Bolwell et al., 1995), and variations in protein phosphorylation patterns (Dietrich et al., 1990;Peck et al., 2001;de Jong et al., 2004). Finally, key mediators such as salicylic acid (SA) accumulate and resistance is induced systemically (Gaffney et al., 1993;Durrant and Dong, 2004;Pieterse and Van Loon, 2004).HR eliminates infected host cells that support continuous plant-pathogen interactions. The plant begins to express a subset of pathogenesis-related (PR)...