Ethylene Modulates the Role of NONEXPRESSOR OF PATHOGENESIS-RELATED GENES1 in Cross Talk between Salicylate and Jasmonate Signaling

被引:230
作者
Leon-Reyes, Antonio [1 ]
Spoel, Steven H. [3 ]
De Lange, Elvira S. [1 ]
Abe, Hiroshi [4 ]
Kobayashi, Masatomo [4 ]
Tsuda, Shinya [5 ]
Millenaar, Frank F. [1 ]
Welschen, Rob A. M. [1 ]
Ritsema, Tita [1 ]
Pieterse, Corne M. J. [1 ,2 ]
机构
[1] Univ Utrecht, Fac Sci, Dept Biol, NL-3508 TB Utrecht, Netherlands
[2] Ctr BioSyst Genom, NL-6700 AB Wageningen, Netherlands
[3] Duke Univ, Dept Biol, Durham, NC 27708 USA
[4] RIKEN, BioResource Ctr, Dept Biol Syst, Tsukuba, Ibaraki 3050074, Japan
[5] Natl Agr Res Ctr, Dept Plant Pathol, Tsukuba, Ibaraki 3058666, Japan
基金
美国国家卫生研究院;
关键词
SYSTEMIC ACQUIRED-RESISTANCE; PLANT DEFENSE RESPONSES; INDUCED DISEASE RESISTANCE; PSEUDOMONAS-SYRINGAE; ARABIDOPSIS-THALIANA; TRANSCRIPTION FACTOR; IMMUNE-RESPONSES; MICROBIAL PATHOGENS; WOUND RESPONSE; FITNESS COSTS;
D O I
10.1104/pp.108.133926
中图分类号
Q94 [植物学];
学科分类号
071001 ;
摘要
The plant hormones salicylic acid (SA), jasmonic acid (JA), and ethylene (ET) play crucial roles in the signaling network that regulates induced defense responses against biotic stresses. Antagonism between SA and JA operates as a mechanism to fine-tune defenses that are activated in response to multiple attackers. In Arabidopsis (Arabidopsis thaliana), NONEXPRESSOR OF PATHOGENESIS-RELATED GENES1 (NPR1) was demonstrated to be required for SA-mediated suppression of JA-dependent defenses. Because ET is known to enhance SA/NPR1-dependent defense responses, we investigated the role of ET in the SA-JA signal interaction. Pharmacological experiments with gaseous ET and the ET precursor 1-aminocyclopropane-1-carboxylic acid showed that ET potentiated SA/NPR1-dependent PATHOGENESIS-RELATED1 transcription, while it rendered the antagonistic effect of SA on methyl jasmonate-induced PDF1.2 and VSP2 expression NPR1 independent. This overriding effect of ET on NPR1 function in SA-JA cross talk was absent in the npr1-1/ein2-1 double mutant, demonstrating that it is mediated via ET signaling. Abiotic and biotic induction of the ET response similarly abolished the NPR1 dependency of the SA-JA signal interaction. Furthermore, JA-dependent resistance against biotic attackers was antagonized by SA in an NPR1-dependent fashion only when the plant-attacker combination did not result in the production of high levels of endogenous ET. Hence, the interaction between ET and NPR1 plays an important modulating role in the fine tuning of the defense signaling network that is activated upon pathogen and insect attack. Our results suggest a model in which ET modulates the NPR1 dependency of SAJA antagonism, possibly to compensate for enhanced allocation of NPR1 to function in SA-dependent activation of PR genes.
引用
收藏
页码:1797 / 1809
页数:13
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