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- Title
The Arabidopsis PARAQUAT RESISTANT2 gene encodes an S-nitrosoglutathione reductase that is a key regulator of cell death.
- Authors
Ruiqiang Chen; Shulan Sun; Chun Wang; Yansha Li; Yan Liang; Fengying An; Chao Li; Haili Dong; Xiaohui Yang; Jian Zhang; Jianru Zuo
- 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.
- Publication
Cell Research, 2009, Vol 19, Issue 12, p1377
- ISSN
1001-0602
- Publication type
Academic Journal
- DOI
10.1038/cr.2009.117