A central role for S-nitrosothiols in plant disease resistance.
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.
Feechan
Angela
A
Institute of Molecular Plant Sciences, School of Biological Sciences, University of Edinburgh, King's Buildings, Edinburgh EH9 3JR, United Kingdom.
Kwon
Eunjung
E
Yun
Byung-Wook
BW
Wang
Yiqin
Y
Pallas
Jacqueline A
JA
Loake
Gary J
GJ
D017360:Arabidopsis / Q000201:enzymology* / Q000235:genetics; D015152:Blotting, Northern; D017931:DNA Primers; D005980:Glutathione Reductase / Q000235:genetics* / Q000378:metabolism; D006651:Histocytochemistry; D007113:Immunity, Innate / Q000235:genetics*; D018613:Microscopy, Confocal; D009154:Mutation / Q000235:genetics; D009693:Nucleic Acid Hybridization; D010935:Plant Diseases / Q000235:genetics* / Q000382:microbiology; D044224:Pseudomonas syringae; D026403:S-Nitrosothiols / Q000378:metabolism*; D020156:Salicylic Acid / Q000378:metabolism; D015398:Signal Transduction / Q000235:genetics*
D017931:DNA Primers; D026403:S-Nitrosothiols; D005980:Glutathione Reductase; D020156:Salicylic Acid