The Expression Patterns of AtBSMT1 and AtSAGT1 Encoding a Salicylic Acid (SA) Methyltransferase and a SA Glucosyltransferase, Respectively, in Arabidopsis Plants with Altered Defense Responses
2009
Song, J.T. (Kyungpook National University, Daegu, Republic of Korea), E-mail: jtsong68@knu.ac.kr | Koo, Y.J. (Seoul National University, Seoul, Republic of Korea) | Park, J.B. (Kyungpook National University, Daegu, Republic of Korea) | Seo, Y.J. (Kyungpook National University, Daegu, Republic of Korea) | Cho, Y.J. (Kyungpook National University, Daegu, Republic of Korea) | Seo, H.S. (Seoul National University, Seoul, Republic of Korea) | Choi, Y.D. (Seoul National University, Seoul, Republic of Korea)
We reported previously that overexpression of a salicylic acid (SA) methyltransferase1 gene from rice (OsBSMT1) or a SA glucosyltransferase1 gene from Arabidopsis thaliana (AtSAGT1) leads to increased susceptibility to Pseudomonas syringae due to reduced SA levels. To further examine their roles in the defense responses, we assayed the transcript levels of AtBSMT1 or AtSAGT1 in plants with altered levels of SA and/or other defense components. These data showed that AtSAGT1 expression is regulated partially by SA, or nonexpressor of pathogenesis related protein1, whereas AtBSMT1 expression was induced in SA-deficient mutant plants. In addition, we produced the transgenic Arabidopsis plants with RNAi-mediated inhibition of AtSAGT1 and isolated a null mutant of AtBSMT1 and then analyzed their phenotypes. A T-DNA insertion mutation in the AtBSMT1 resulted in reduced methyl salicylate (MeSA) levels upon P. syringae infection. However, accumulation of SA and glucosyl SA was similar in both the atbsmt1 and wild-type plants, indicating the presence of another SA methyltransferase or an alternative pathway for MeSA production. The AtSAGT1-RNAi line exhibited no altered phenotypes upon pathogen infection, compared to wild-type plants, suggesting that (an)other SA glucosyltransferase(s) in Arabidopsis plants may be important for the pathogenesis of P. syringae.
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