Information de reference pour ce titreAccession Number: | 00006056-201206140-00048.
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Author: | Fu, Zheng Qing 1,6; Yan, Shunping 1,6; Saleh, Abdelaty 1,6; Wang, Wei 1; Ruble, James 2; Oka, Nodoka 3; Mohan, Rajinikanth 1; Spoel, Steven H. 4; Tada, Yasuomi 5; Zheng, Ning 2; Dong, Xinnian 1
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Institution: | (1)Howard Hughes Medical Institute-Gordon and Betty Moore Foundation, Department of Biology, PO Box 90338, Duke University, Durham, North Carolina 27708, USA (2)Howard Hughes Medical Institute, Department of Pharmacology, University of Washington, PO Box 357280, Seattle, Washington 98195, USA (3)Faculty of Agriculture, Kagawa University, Miki, Kagawa 761-0795, Japan (4)Institute of Molecular Plant Sciences, University of Edinburgh, Edinburgh EH9 3JR, UK (5)Life Science Research Center, Institute of Research Promotion, Kagawa University, 2393 Ikenobe, Miki-cho, Kita-gun, Kagawa 761-0795, Japan (6)These authors contributed equally to this work.
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Title: | NPR3 and NPR4 are receptors for the immune signal salicylic acid in plants.[Article]
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Source: | Nature. 486(7402):228-232, June 14, 2012.
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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.
(C) 2012 Nature Publishing Group
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Language: | English.
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Document Type: | ARTICLE.
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Journal Subset: | Life & Biomedical Sciences. Science.
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ISSN: | 0028-0836
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NLM Journal Code: | 0410462, nsc
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DOI Number: | https://dx.doi.org/10.1038/natur...- ouverture dans une nouvelle fenêtre
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