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Published on January 28, 2009; 10.1104/pp.108.133926

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Received December 9, 2008
Accepted January 25, 2009

Ethylene Modulates the Role of NPR1 in Cross-Talk Between Salicylate and Jasmonate Signaling

Antonio Leon-Reyes , Steven H. Spoel , Elvira S. De Lange , Hiroshi Abe , Masatomo Kobayashi , Shinya Tsuda , Frank F. Millenaar , Rob A.M. Welschen , Tita Ritsema , and Corne M.J. Pieterse *

Plant-Microbe Interactions, Department of Biology, Faculty of Science, Utrecht University, P.O. Box 800.56, 3508 TB Utrecht, the Netherlands; Department of Biology, Duke University, Durham, NC 27708-1000, U.S.A; Department of Biological Systems, RIKEN BioResource Center, Tsukuba 305-0074, Japan; Department of Plant Pathology, National Agricultural Research Center, Tsukuba 305-8666, Japan; Plant Ecophysiology, Department of Biology, Faculty of Science, Utrecht University, P.O.Box 800.84, 3508 TB Utrecht, the Netherlands

* Corresponding author; email: C.M.J.Pieterse{at}uu.nl.

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, 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 PR-1 transcription, while it rendered the antagonistic effect of SA on methyl-JA-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 SA-JA antagonism, possibly to compensate for enhanced allocation of NPR1 to function in SA-dependent activation of PR genes.




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