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PLANTS INTERACTING WITH OTHER ORGANISMS

Vitamin B₁ Functions as an Activator of Plant Disease Resistance¹

School of Agricultural Biotechnology and Center for Agricultural Biomaterials, Seoul National University, Seoul 151–742, Korea

Vitamin B₁ (thiamine) is an essential nutrient for humans. Vitamin B₁ 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 Ca²⁺-related signaling pathways. The findings provide a novel paradigm for developing alternative strategies for the control of plant diseases.

² Present address: National Institute of Agricultural Biotechnology, Suwon 441–100, Korea.

Article, publication date, and citation information can be found at www.plantphysiol.org/cgi/doi/10.1104/pp.104.058693.

^* Corresponding author; e-mail yonglee{at}snu.ac.kr; fax 82–2–873–2317.

Received December 21, 2004; returned for revision March 28, 2005; accepted April 4, 2005.

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