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Antagonistic Interaction between Systemic Acquired Resistance and the Abscisic Acid–Mediated Abiotic Stress Response in Arabidopsis^[W]

^a Plant Acquired Immunity Research Unit, Advanced Science Institute, RIKEN, Wako, Saitama 351-0198, Japan
^b Mayekawa MFG. Co., Moriya, Ibaraki 302-0118, Japan
^c Department of Bioscience, Fukui Prefectural University, Fukui 910-1195, Japan
^d Growth Regulation Research Group, RIKEN Plant Science Center, Yokohama, Kanagawa 230-0045, Japan
^e Plant Functional Genomics Research Group, RIKEN Plant Science Center, Yokohama, Kanagawa 230-0045, Japan
^f Gene Discovery Research Group, RIKEN Plant Science Center, Yokohama, Kanagawa 230-0045, Japan
^g Department of Applied Biological Chemistry, University of Tokyo, Tokyo 113-8657, Japan
^h Metabolic Function Research Group, RIKEN Plant Science Center, Yokohama, Kanagawa 230-0045, Japan
ⁱ Environmental Molecular Biology Laboratory, Discovery Research Institute, RIKEN, Wako, Saitama 351-0198, Japan
^j RIKEN Plant Science Center, RIKEN Yokohama Institute, Yokohama, Kanagawa 230-0045, Japan

¹ Address correspondence to nakashi{at}riken.jp.

Systemic acquired resistance (SAR) is a potent innate immunity system in plants that is effective against a broad range of pathogens. SAR development in dicotyledonous plants, such as tobacco (Nicotiana tabacum) and Arabidopsis thaliana, is mediated by salicylic acid (SA). Here, using two types of SAR-inducing chemicals, 1,2-benzisothiazol-3(2H)-one1,1-dioxide and benzo(1,2,3)thiadiazole-7-carbothioic acid S-methyl ester, which act upstream and downstream of SA in the SAR signaling pathway, respectively, we show that treatment with abscisic acid (ABA) suppresses the induction of SAR in Arabidopsis. In an analysis using several mutants in combination with these chemicals, treatment with ABA suppressed SAR induction by inhibiting the pathway both upstream and downstream of SA, independently of the jasmonic acid/ethylene-mediated signaling pathway. Suppression of SAR induction by the NaCl-activated environmental stress response proved to be ABA dependent. Conversely, the activation of SAR suppressed the expression of ABA biosynthesis–related and ABA-responsive genes, in which the NPR1 protein or signaling downstream of NPR1 appears to contribute. Therefore, our data have revealed that antagonistic crosstalk occurs at multiple steps between the SA-mediated signaling of SAR induction and the ABA-mediated signaling of environmental stress responses.

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