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Abscisic Acid Interacts Antagonistically with Salicylic Acid Signaling Pathway in Rice-Magnaporthe grisea Interaction
- Jiang, Chang-Jie, Shimono, Masaki, Sugano, Shoji, Kojima, Mikiko, Yazawa, Katsumi, Yoshida, Riichiro, Inoue, Haruhiko, Hayashi, Nagao, Sakakibara, Hitoshi, Takatsuji, Hiroshi
- Molecular plant-microbe interactions 2010 v.23 no.6 pp. 791-798
- Oryza sativa, rice, grain crops, Magnaporthe grisea, plant pathogenic fungi, blast disease, abscisic acid, salicylic acid, resistance mechanisms, antagonists, biochemical pathways, signal transduction, plant hormones, exogenous sources, foliar application, gene expression regulation, transcription (genetics), hyphae, conidia, culture media
- Plant hormones play pivotal signaling roles in plant-pathogen interactions. Here, we report characterization of an antagonistic interaction of abscisic acid (ABA) with salicylic acid (SA) signaling pathways in the rice-Magnaporthe grisea interaction. Exogenous application of ABA drastically compromised the rice resistance to both compatible and incompatible M. grisea strains, indicating that ABA negatively regulates both basal and resistance gene-mediated blast resistance. ABA markedly suppressed the transcriptional upregulation of WRKY45 and OsNPR1, the two key components of the SA signaling pathway in rice, induced by SA or benzothiadiazole or by blast infection. Overexpression of OsNPR1 or WRKY45 largely negated the enhancement of blast susceptibility by ABA, suggesting that ABA acts upstream of WRKY45 and OsNPR1 in the rice SA pathway. ABA-responsive genes were induced during blast infection in a pattern reciprocal to those of WRKY45 and OsPR1b in the compatible rice-blast interaction but only marginally in the incompatible one. These results suggest that the balance of SA and ABA signaling is an important determinant for the outcome of the rice-M. grisea interaction. ABA was detected in hyphae and conidia of M. grisea as well as in culture media, implying that blast-fungus-derived ABA could play a role in triggering ABA signaling at host infection sites.