NPR3 and NPR4 are receptors for the immune signal salicylic acid in plants

Zheng Qing Fu, Shunping Yan, Abdelaty Saleh, Wei Wang, James Ruble, Nodoka Oka, Rajinikanth Mohan, Steven H. Spoel, Yasuomi Tada, Ning Zheng and Xinnian Dong ()
Additional contact information
Zheng Qing Fu: Howard Hughes Medical Institute–Gordon and Betty Moore Foundation, PO Box 90338, Duke University
Shunping Yan: Howard Hughes Medical Institute–Gordon and Betty Moore Foundation, PO Box 90338, Duke University
Abdelaty Saleh: Howard Hughes Medical Institute–Gordon and Betty Moore Foundation, PO Box 90338, Duke University
Wei Wang: Howard Hughes Medical Institute–Gordon and Betty Moore Foundation, PO Box 90338, Duke University
James Ruble: Howard Hughes Medical Institute, University of Washington, PO Box 357280, Seattle, Washington 98195, USA
Nodoka Oka: Faculty of Agriculture, Kagawa University, Miki, Kagawa 761-0795, Japan
Rajinikanth Mohan: Howard Hughes Medical Institute–Gordon and Betty Moore Foundation, PO Box 90338, Duke University
Steven H. Spoel: Institute of Molecular Plant Sciences, University of Edinburgh, Edinburgh EH9 3JR, UK
Yasuomi Tada: Life Science Research Center, Institute of Research Promotion, Kagawa University, 2393 Ikenobe, Miki-cho, Kita-gun, Kagawa 761-0795, Japan
Ning Zheng: Howard Hughes Medical Institute, University of Washington, PO Box 357280, Seattle, Washington 98195, USA
Xinnian Dong: Howard Hughes Medical Institute–Gordon and Betty Moore Foundation, PO Box 90338, Duke University

Nature, 2012, vol. 486, issue 7402, 228-232

Abstract: Abstract Salicylic acid (SA) is a plant immune signal produced after pathogen challenge to induce systemic acquired resistance. It is the only major plant hormone for which the receptor has not been firmly identified. Systemic acquired resistance in Arabidopsis requires the transcription cofactor nonexpresser of PR genes 1 (NPR1), the degradation of which acts as a molecular switch. Here we show that the NPR1 paralogues NPR3 and NPR4 are SA receptors that bind SA with different affinities. NPR3 and NPR4 function as adaptors of the Cullin 3 ubiquitin E3 ligase to mediate NPR1 degradation in an SA-regulated manner. Accordingly, the Arabidopsis npr3 npr4 double mutant accumulates higher levels of NPR1, and is insensitive to induction of systemic acquired resistance. Moreover, this mutant is defective in pathogen effector-triggered programmed cell death and immunity. Our study reveals the mechanism of SA perception in determining cell death and survival in response to pathogen challenge.

Date: 2012
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DOI: 10.1038/nature11162

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