Erratum: Involvement of sphingoid bases in mediating reactive oxygen intermediate production and programmed cell death in Arabidopsis

Shi, Lihua; Bielawski, Jacek; Mu, Jinye; Dong, Haili; Teng, Chong; Zhang, Jian; Yang, Xiaohui; Tomishige, Nario; Hanada, Kentaro; Hannun, Yusuf A.; Zuo, Jianru

doi:10.1038/cr.2008.22

Cited by 25 publications

(59 citation statements)

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“…Because a major physiological effect of paraquat is the induction of superoxide and free radicals in plant cells, it is reasonable to assume that PAR2 functions downstream of superoxide to regulate cell death. This view is supported by the observation that par2-1 displays resistance to FB 1 , which also induces the formation of ROS [8,9,11].…”

Section: Discussionsupporting

confidence: 70%

“…This result indicates that the paraquatinduced production of superoxide does not require PAR2, which likely acts downstream of ROS to regulate cell death. In agreement with this notion, par2-1 also showed resistance to FB 1 ( Figure 1D), a fungal toxin that can efficiently induce PCD in plants, likely via regulating ROS generation [8,9,11,14].…”

Section: The Par2-1 Mutant Phenotypesupporting

confidence: 63%

“…Detection of cell death, superoxide and hydrogen peroxide was carried out by staining leaves with Evans blue, nitroblue tetrazolium (NBT) and 3,3′-diaminobenzidine, respectively, essentially as previously described [11]. All experiments were repeated for 3-5 times (biological repeats), and 10-15 rosette leaves collected from multiple seedlings (4-5-week-old) were analyzed in each experiment.…”

Section: Analysis Of Cell Death Superoxide Hydrogen Peroxide and Numentioning

confidence: 99%

“…Whereas FBR6 and FBR12 encode a plant-specific transcription factor, AtSPL14, and a eukaryotic translation initiation factor 5A, respectively [10,12], FBR11 encodes a subunit of serine palmitoyltransferase that catalyzes the first rate-limiting reaction of sphingolipid de novo synthesis [11,13]. Although sphingolipid-regulated cell death has been attributed to ROS production [11,14], the molecular link between these two classes of signaling molecules remains unclear.…”

Section: Introductionmentioning

confidence: 99%

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

et al. 2009

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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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Section: Discussionsupporting

confidence: 70%

Section: The Par2-1 Mutant Phenotypesupporting

confidence: 63%

Section: Analysis Of Cell Death Superoxide Hydrogen Peroxide and Numentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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

et al. 2009

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“…Treatment with AAL toxin or fumonisin B 1 led to the accumulation of free sphingoid bases such as 3-ketodihydrosphinganine and dihydrosphinganine, which in turn lead to cell death. 42,43 Recently, Shi et al, 44 reported that the Arabidopsis mutant fbr 11-1 (fumonisin B 1 resistant 11-1), which is incapable of initiating PCD when the mutant is treated with fumonisin B 1 , a specific inhibitor of ceramide synthase, encodes a long-chain base 1 (LCB1) subunit of serine palmitoyltransferase (SPT), which catalyzes the first step in the sphingolipid biosynthetic pathway. The authors also presented data that the free sphingoid bases dihydrosphingosine, phytosphingosine and sphingosine induce PCD whereas dihydrosphingosine-1-phosphate blocked sphinosine-induced PCD in a dose-dependent manner.…”

Section: A Role For Sphingolipids In Pcdmentioning

confidence: 99%

Lesion mimic mutants

Moeder

Yoshioka²

2008

Plant Signaling & Behavior

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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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Erratum: Involvement of sphingoid bases in mediating reactive oxygen intermediate production and programmed cell death in Arabidopsis

Cited by 25 publications

References 0 publications

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

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

Lesion mimic mutants

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

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