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

Chen, Ruiqiang; Sun, Shan; Wang, Chun; Li, Yansha; Liang, Yan; An, Fengying; Li, Chao; Dong, Haili; Yang, Xiaohui; Zhang, Jian; Zuo, Jianru

doi:10.1038/cr.2009.117

Cited by 167 publications

(175 citation statements)

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“…Mutation in PHB3 abort NO accumulation but does not affect H 2 O 2 signaling. Further substantiating the link between ROS and NO during cell death is the recent positional cloning of PARAQUAT RESISTANT2 gene in Arabidopsis, which encodes an S-nitrosoglutathione reductase (Chen et al 2009). Positional cloning of the atr mutants will help to understand the intricate mechanisms of cell death tolerance in Arabidopsis.…”

Section: Molecular Analysis Of Mutants Exposed To At-induced Oxidativmentioning

confidence: 99%

Isolation and characterization of Arabidopsis mutants with enhanced tolerance to oxidative stress

Qureshi

Radeva²,

Genkov³

et al. 2010

Acta Physiol Plant

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We have previously reported a method for isolation of mutants with enhanced tolerance to the fungal AAL toxin and given a detailed characterization of atr1 (AAL toxin resistant, Gechev et al. in Biochem Biophys Res Commun 375:639-644, 2008). Herewith, we report eight more mutants with enhanced tolerance to the AAL toxin. Phenotypic analysis showed that six of the mutants were reduced in size compared with their original background loh2. Furthermore, atr2 showed delayed flowering and senescence. The mutants were also evaluated for oxidative stress tolerance by growing them on ROS-inducing media supplemented with either aminotriazole or paraquat, generating, respectively, H 2 O 2 or superoxide radicals. Oxidative stress, confirmed by induction of the marker genes, HIGH AFFINITY NITRATE TRANSPORTER At1G08090 and HEAT SHOCK PROTEIN 17 At3G46230, inhibited growth of all lines. However, while the original background loh2 developed necrotic lesions and died rapidly on ROS-inducing plant growth media, atr1, atr2, atr7 and atr9 remained green and viable. The tolerance against oxidative stress-induced cell death was confirmed by fresh weight and chlorophyll measurements. Real-time PCR analysis revealed that the expression of the EXTENSIN gene At5G46890, previously shown to be downregulated by aminotriazole in atr1, was repressed in all lines, consistent with the growth inhibition induced by oxidative stress. Taken together, the data indicate a complex link between growth, development and oxidative stress tolerance and indicates that growth inhibition can be uncoupled from oxidative stress-induced cell death.

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Section: Molecular Analysis Of Mutants Exposed To At-induced Oxidativmentioning

confidence: 99%

Isolation and characterization of Arabidopsis mutants with enhanced tolerance to oxidative stress

Qureshi

Radeva²,

Genkov³

et al. 2010

Acta Physiol Plant

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“…NO overaccumulates in Arabidopsis gsnor1(S-nitrosoglutathione reductase 1)/hot5 (sensitive to hot temperatures 5)/par2 (paraquat resistant 2) mutant plants that are impaired in the GSNO reductase gene (32)(33)(34). The gsnor1-3 mutant is hypersensitive to heat stress (33) and bacterial pathogen (28,31), but is more resistant to oxidative stress (34).…”

mentioning

confidence: 99%

Nitric oxide negatively regulates abscisic acid signaling in guard cells by S-nitrosylation of OST1

Wang¹,

Hou³

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

315

212

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The phytohormone abscisic acid (ABA) plays important roles in plant development and adaptation to environmental stress. ABA induces the production of nitric oxide (NO) in guard cells, but how NO regulates ABA signaling is not understood. Here, we show that NO negatively regulates ABA signaling in guard cells by inhibiting open stomata 1 (OST1)/sucrose nonfermenting 1 (SNF1)-related protein kinase 2.6 (SnRK2.6) through S-nitrosylation. We found that SnRK2.6 is S-nitrosylated at cysteine 137, a residue adjacent to the kinase catalytic site. Dysfunction in the S-nitrosoglutathione (GSNO) reductase (GSNOR) gene in the gsnor1-3 mutant causes NO overaccumulation in guard cells, constitutive S-nitrosylation of SnRK2.6, and impairment of ABA-induced stomatal closure. Introduction of the Cys137 to Ser mutated SnRK2.6 into the gsnor1-3/ ost1-3 double-mutant partially suppressed the effect of gsnor1-3 on ABA-induced stomatal closure. A cysteine residue corresponding to Cys137 of SnRK2.6 is present in several yeast and human protein kinases and can be S-nitrosylated, suggesting that the S-nitrosylation may be an evolutionarily conserved mechanism for protein kinase regulation.A bscisic acid (ABA) plays critical roles in seed dormancy and germination, plant growth, and adaptation to environmental challenges (1, 2). Stresses, such as drought and high salt conditions, increase ABA concentration in plants as a result of ABA biosynthesis or ABA release from its inactive, conjugated forms (3). In the presence of ABA, the ABA receptors in the PYR1 (Pyrabactin Resistance 1)/PYL (PYR1-Like)/RCAR (Regulatory Component of ABA receptor) protein family bind to and inhibit the activity of clade A protein phosphatase 2Cs (PP2Cs), which are considered as coreceptors and negative regulators of ABA signaling (4-6). This process then results in the release of sucrose nonfermenting 1 (SNF1)-related protein kinase 2s (SnRK2s) from suppression by the PP2Cs. As central components of the ABA signaling pathway, the activated SnRK2s phosphorylate dozens of downstream effectors to regulate various physiological processes, including stomatal closure, root growth and development, seed dormancy, seed germination, and flowering (7).As the gateway for photosynthetic CO 2 uptake and transpirational water loss, stomata are critical for plant growth and physiology (8). ABA regulates stomatal movement and mutations in ABA biosynthesis genes (9), or in the PYL or SnRK2.6 (also known as OST1) genes cause open-stomata phenotypes (10). On the other hand, dysfunction of the PP2Cs or overexpression of RCAR1/PYL9 causes stomatal closure (5). Among the three SnRK2s, SnRK2.2, -2.3, and -2.6, which are most important for ABA signaling, SnRK2.6 is preferentially expressed in guard cells and plays a critical role in stomatal regulation, whereas SnRK2.2 and -2.3 are mainly expressed in seeds and young seedlings and are thus more important for seed germination and seedling growth (4, 11). SnRK2.6 phosphorylates the slow (S-type) anion channel associated 1 and inward potass...

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“…This study provided evidence that SNO metabolism controlled by GSNOR had a key role in plant disease resistance. Further studies have since revealed that GSNOR appears to be a key regulator of cell death (9) and is also required for thermotolerance (22). Various studies discussed in the following section have also shown that S-nitrosylation of specific proteins is increased in gsnor1-3 mutant plants.…”

Section: S-nitrosoglutathione-reductase and S-nitrosylationmentioning

confidence: 92%

Synthesis of Redox-Active Molecules and Their Signaling Functions During the Expression of Plant Disease Resistance

Skelly

Loake

2013

Antioxidants & Redox Signaling

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Significance: Activation of immune responses in plants is associated with a parallel burst of both reactive oxygen intermediates (ROIs) and nitric oxide (NO). The mechanisms by which these small redox-active molecules are synthesized and their signaling functions are critical for plants to defend themselves against pathogen infection. Recent Advances: The synthesis of apoplastic ROIs by plants after pathogen recognition has long been attributed to membrane-bound NAPDH oxidases. However, the emerging data suggest a role for other enzymes in various subcellular locations in ROI production after defense activation. It is becoming widely appreciated that NO exerts its biochemical function through the S-nitrosylation of reactive cysteine thiols on target proteins, constituting a key post-translational modification. Recent evidence suggests that S-nitrosylation of specific defense-related proteins regulates their activity. Critical Issues: The source(s) of NO production after pathogen recognition remain(s) poorly understood. Some NO synthesis can be attributed to the activity of nitrate reductase but to date, no nitric oxide synthase (NOS) has been identified in higher plants. However, the signaling functions of S-nitrosylation are becoming more apparent and thus dissecting the molecular machinery underpinning this redox-based modification is vital to further our understanding of plant disease resistance. Future Directions: In addition to identifying new contributors to the oxidative burst, the discovery of an NOS in higher plants would significantly move the field forward. Since S-nitrosylation has now been confirmed to play various roles in immune signaling, this redox-based modification is a potential target to exploit for improving disease resistance in crop species. Antioxid. Redox Signal. 19,[990][991][992][993][994][995][996][997]

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

Cited by 167 publications

References 65 publications

Isolation and characterization of Arabidopsis mutants with enhanced tolerance to oxidative stress

Isolation and characterization of Arabidopsis mutants with enhanced tolerance to oxidative stress

Nitric oxide negatively regulates abscisic acid signaling in guard cells by S-nitrosylation of OST1

Synthesis of Redox-Active Molecules and Their Signaling Functions During the Expression of Plant Disease Resistance

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