Open AccessA central role forS-nitrosothiols in plant disease resistance
Author(s) -
Angela Feechan,
Eunjung Kwon,
ByungWook Yun,
Yiqin Wang,
Jacqueline A. Pallas,
Gary J. Loake
Publication year - 2005
Publication title -
proceedings of the national academy of sciences of the united states of america
Language(s) - English
Resource type - Journals
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.0501456102
Subject(s) - salicylic acid , s nitrosylation , arabidopsis , biology , microbiology and biotechnology , arabidopsis thaliana , systemic acquired resistance , activator (genetics) , plant disease resistance , immune system , reductase , mutant , plant immunity , signal transduction , function (biology) , plant defense against herbivory , biochemistry , enzyme , gene , genetics , cysteine
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.