Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 102, Issue 22, Pages 8054-8059Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.0501456102
Keywords
S-nitrosylation; salicylic acid; nitric oxide
Categories
Funding
- Biotechnology and Biological Sciences Research Council [P20067] Funding Source: Medline
- NCHHSTP CDC HHS [H75 PS003121] Funding Source: Medline
- Biotechnology and Biological Sciences Research Council [P20067] Funding Source: researchfish
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Animal 5-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.
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