S-Nitrosoglutathione reductase (GSNOR) mediates the biosynthesis of jasmonic acid and ethylene induced by feeding of the insect herbivore Manduca sexta and is important for jasmonate-elicited responses in Nicotiana attenuata. J Exp Bot

Department of Molecular Ecology, Max Planck Institute for Chemical Ecology, Hans-Knoell-Str. 8, D-07745 Jena, Germany.
Journal of Experimental Botany (Impact Factor: 5.53). 05/2011; 62(13):4605-16. DOI: 10.1093/jxb/err171
Source: PubMed


S-nitrosoglutathione reductase (GSNOR) reduces the nitric oxide (NO) adduct S-nitrosoglutathione (GSNO), an essential reservoir for NO bioactivity. In plants, GSNOR has been found to be important in
resistance to bacterial and fungal pathogens, but whether it is also involved in plant–herbivore interactions was not known.
Using a virus-induced gene silencing (VIGS) system, the activity of GSNOR in a wild tobacco species, Nicotiana attenuata, was knocked down and the function of GSNOR in defence against the insect herbivore Manduca sexta was examined. Silencing GSNOR decreased the herbivory-induced accumulation of jasmonic acid (JA) and ethylene, two important phytohormones regulating plant
defence levels, without compromising the activity of two mitogen-activated protein kinases (MAPKs), salicylic acid-induced
protein kinase (SIPK) and wound-induced protein kinase (WIPK). Decreased activity of trypsin proteinase inhibitors (TPIs)
were detected in GSNOR-silenced plants after simulated M. sexta feeding and bioassays indicated that GSNOR-silenced plants have elevated susceptibility to M. sexta attack. Furthermore, GSNOR is required for methyl jasmonate (MeJA)-induced accumulation of defence-related secondary metabolites
(TPI, caffeoylputrescine, and diterpene glycosides) but is not needed for the transcriptional regulation of JAZ3 (jasmonate ZIM-domain 3) and TD (threonine deaminase), indicating that GSNOR mediates certain but not all jasmonate-inducible responses. This work highlights the important role
of GSNOR in plant resistance to herbivory and jasmonate signalling and suggests the potential involvement of NO in plant–herbivore
interactions. Our data also suggest that GSNOR could be a target of genetic modification for improving crop resistance to

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    • "). Meanwhile, the current data confirmed previous observations (Wünsche et al. 2011) showing that there is no direct correlation between transcript levels of GSNOR and its activity (Fig. 3b). "
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    • "Thus, it is possible that BAK1 somehow influences the activity of certain JA biosynthetic enzymes on a post-transcriptional level (Yang et al., 2011a, 2011b). GSNOR affects the level of nitrosoglutathione (GSNO), a source of nitric oxide (NO); thus, GSNOR may influence the activity of certain JA biosynthetic enzymes by changing their nitrosylation status (Wunsche et al., 2011b). Supporting this scenario, at least one enzyme in the oxylipin pathway for JA biosynthesis, allene-oxide cyclase (AOC), has been identified to be a nitrosylation target (Romero-Puertas et al., 2008). "
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    ABSTRACT: The plant hormone jasmonic acid (JA) plays a central role in plant defense against herbivores. Herbivore damage elicits a rapid and transient JA burst in the wounded leaves and JA functions as a signal to mediate the accumulation of various secondary metabolites that confer resistance to herbivores. Nicotiana attenuata is a wild tobacco species that inhabits western North America. More than fifteen years of study and its unique interaction with the specialist herbivore insect Manduca sexta have made this plant one of the best models for studying plant-herbivore interactions. Here we review the recent progress in understanding the elicitation of JA accumulation by herbivore-specific elicitors, the regulation of JA biosynthesis, JA signaling, and the herbivore-defense traits in N. attenuata.
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    • "Caterpillar herbivory also had significantly lower oxidized GSSG levels at 35 min post-herbivory; this effect was not salivary-dependent. Cellular glutathione–ascorbate metabolites levels and/or redox balance are involved in plant defense against pathogens or herbivores (Mou et al., 2003; Ball et al., 2004; Parisy et al., 2007; Schlaeppi et al., 2008; Wünsche et al., 2011; Espunya et al., 2012). The majority of experiments investigating changes in redox metabolites in response to stress (wound, herbivory, pathogens) characterize long-term changes in the cellular oxidative status (Fodor et al., 1997; Mou et al., 2003; Ball et al., 2004; Mateo et al., 2006; Schlaeppi et al., 2008; Gfeller et al., 2011). "
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    ABSTRACT: Plant responses to insect herbivory are regulated through complex, hormone-mediated interactions. Some caterpillar species have evolved strategies to manipulate this system by inducing specific pathways that suppress plant defense responses. Effectors in the labial saliva (LS) secretions of Spodoptera exigua caterpillars are believed to induce the salicylic acid (SA) pathway to interfere with the jasmonic acid (JA) defense pathway; however, the mechanism underlying this subversion is unknown. Since noctuid caterpillar LS contains enzymes that may affect cellular redox balance, this study investigated rapid changes in cellular redox metabolites within 45 min after herbivory. Caterpillar LS is involved in suppressing the increase in oxidative stress that was observed in plants fed upon by caterpillars with impaired LS secretions. To further understand the link between cellular redox balance and plant defense responses, marker genes of SA, JA and ethylene (ET) pathways were compared in wildtype, the glutathione-compromised pad2-1 mutant and the tga2/5/6 triple mutant plants. AtPR1 and AtPDF1.2 showed LS-dependent expression that was alleviated in the pad2-1 and tga2/5/6 triple mutants. In comparison, the ET-dependent genes ERF1 expression showed LS-associated changes in both wildtype and pad2-1 mutant plants and the ORA 59 marker AtHEL had increased expression in response to herbivory, but a LS-dependent difference was not noted. These data support the model that there are SA/NPR1-, glutathione-dependent and ET-, glutathione-independent mechanisms leading to LS-associated suppression of plant induced defenses.
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