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A Central Role for S-Nitrosothiols in Plant Disease Resistance
Angela Feechan, Eunjung Kwon, Byung-Wook Yun, Yiqin Wang, Jacqueline A. Pallas, Gary J. Loake and Brian J. Staskawicz
Proceedings of the National Academy of Sciences of the United States of America
Vol. 102, No. 22 (May 31, 2005), pp. 8054-8059
Published by: National Academy of Sciences
Stable URL: http://www.jstor.org/stable/3375717
Page Count: 6
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Animal S-nitrosoglutathione reductase (GSNOR) governs the extent of cellular S-nitrosylation, a key redox-based posttranslational modification. Mutations in AtGSNOR1, an Arabidopsis thaliana GSNOR, modulate the extent of cellular S-nitrosothiol (SNO) formation in this model plant species. Loss of AtGSNOR1 function increased SNO levels, disabling plant defense responses conferred by distinct resistance (R) gene subclasses. Furthermore, in the absence of AtGSNOR1, both basal and nonhost disease resistance are also compromised. Conversely, increased AtGSNOR1 activity reduced SNO formation, enhancing protection against ordinarily virulent microbial pathogens. Here we demonstrate that AtGSNOR1 positively regulates the signaling network controlled by the plant immune system activator, salicylic acid. This contrasts with the function of this enzyme in mice during endotoxic shock, where GSNOR antagonizes inflammatory responses. Our data imply SNO formation and turnover regulate multiple modes of plant disease resistance.
Proceedings of the National Academy of Sciences of the United States of America © 2005 National Academy of Sciences