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The Arabidopsis PARAQUAT RESISTANT2 gene encodes an S-nitrosoglutathione reductase that is a key regulator of cell death.

Authors
  • Chen, Ruiqiang1
  • Sun, Shulan
  • Wang, Chun
  • Li, Yansha
  • Liang, Yan
  • An, Fengying
  • Li, Chao
  • Dong, Haili
  • Yang, Xiaohui
  • Zhang, Jian
  • Zuo, Jianru
  • 1 State Key Laboratory of Plant Genomics and National Plant Gene Research Center (Beijing), Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing 100101, China. , (China)
Type
Published Article
Journal
Cell Research
Publisher
Springer Nature
Publication Date
Dec 01, 2009
Volume
19
Issue
12
Pages
1377–1387
Identifiers
DOI: 10.1038/cr.2009.117
PMID: 19806166
Source
Medline
License
Unknown

Abstract

Metabolism of S-nitrosoglutathione (GSNO), a major biologically active nitric oxide (NO) species, is catalyzed by the evolutionally conserved GSNO reductase (GSNOR). Previous studies showed that the Arabidopsis GSNOR1/HOT5 gene regulates salicylic acid signaling and thermotolerance by modulating the intracellular S-nitrosothiol level. Here, we report the characterization of the Arabidopsis paraquat resistant2-1 (par2-1) mutant that shows an anti-cell death phenotype. The production of superoxide in par2-1 is comparable to that of wild-type plants when treated by paraquat (1,1'-dimethyl-4,4'-bipyridinium dichloride), suggesting that PAR2 acts downstream of superoxide to regulate cell death. PAR2, identified by positional cloning, is shown to be identical to GSNOR1/HOT5. The par2-1 mutant carries a missense mutation in a highly conserved glycine, which renders the mutant protein unstable. Compared to wild type, par2-1 mutant has a higher NO level, as revealed by staining with 4,5-diaminofluorescein diacetate. Consistent with this result, wild-type plants treated with an NO donor display resistance to paraquat. Interestingly, the GSNOR1/HOT5/PAR2 protein level, other than its steady-state mRNA level, is induced by paraquat, but is reduced by NO donors. Taken together, these results suggest that GSNOR1/HOT5/PAR2 plays an important role in regulating cell death in plant cells through modulating intracellular NO level.

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