Antagonistic interaction between systemic acquired resistance and the abscisic acid-mediated abiotic stress response in Arabidopsis.
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.
Yasuda
Michiko
M
Plant Acquired Immunity Research Unit, Advanced Science Institute, RIKEN, Wako, Saitama 351-0198, Japan.
Ishikawa
Atsushi
A
Jikumaru
Yusuke
Y
Seki
Motoaki
M
Umezawa
Taishi
T
Asami
Tadao
T
Maruyama-Nakashita
Akiko
A
Kudo
Toshiaki
T
Shinozaki
Kazuo
K
Yoshida
Shigeo
S
Nakashita
Hideo
H
D000040:Abscisic Acid / Q000378:metabolism / Q000494:pharmacology*; D017360:Arabidopsis / Q000187:drug effects* / Q000235:genetics / Q000378:metabolism; D029681:Arabidopsis Proteins / Q000235:genetics; D003517:Cyclopentanes / Q000378:metabolism / Q000494:pharmacology; D004351:Drug Resistance; D005030:Ethylenes / Q000378:metabolism / Q000494:pharmacology; D018506:Gene Expression Regulation, Plant / Q000187:drug effects; D009154:Mutation; D020411:Oligonucleotide Array Sequence Analysis; D054883:Oxylipins / Q000378:metabolism / Q000494:pharmacology; D010937:Plant Growth Regulators / Q000378:metabolism / Q000494:pharmacology; D030821:Plants, Genetically Modified / Q000187:drug effects / Q000235:genetics / Q000378:metabolism; D020156:Salicylic Acid / Q000378:metabolism / Q000494:pharmacology; D015398:Signal Transduction; D013438:Sulfhydryl Compounds / Q000494:pharmacology; D013830:Thiadiazoles / Q000494:pharmacology; D020691:rab GTP-Binding Proteins / Q000235:genetics
C414667:1,2-benzodithiol-3-one-1,1-dioxide; D029681:Arabidopsis Proteins; D003517:Cyclopentanes; D005030:Ethylenes; D054883:Oxylipins; D010937:Plant Growth Regulators; D013438:Sulfhydryl Compounds; D013830:Thiadiazoles; C078703:rab18 protein, Arabidopsis; C077262:PR-1 protein, Arabidopsis; C011006:jasmonic acid; D000040:Abscisic Acid; C099403:S-methyl benzo(1,2,3)thiadiazole-7-carbothioate; D020691:rab GTP-Binding Proteins; D020156:Salicylic Acid