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« Previous Abstract"Sex pheromones of two Asian moths (Creatonotos transiens, C. gangis; Lepidoptera--Arctiidae): behavior, morphology, chemistry and electrophysiology"    Next AbstractSilencing NOA1 elevates herbivory-induced jasmonic acid accumulation and compromises most of the carbon-based defense metabolites in Nicotiana attenuata(F) »

J Exp Bot


Title: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
Author(s):Wunsche H; Baldwin IT; Wu J;
Address:"Department of Molecular Ecology, Max Planck Institute for Chemical Ecology, Hans-Knoell-Str. 8, D-07745 Jena, Germany"
Journal Title:J Exp Bot
Year:2011
Volume:20110527
Issue:13
Page Number:4605 - 4616
DOI: 10.1093/jxb/err171
ISSN/ISBN:1460-2431 (Electronic) 0022-0957 (Print) 0022-0957 (Linking)
Abstract:"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 herbivores"
Keywords:"Acetates/pharmacology Aldehyde Oxidoreductases/genetics/*metabolism Animals Cyclopentanes/*metabolism/pharmacology Ethylenes/*metabolism Gene Expression Regulation, Enzymologic/drug effects Gene Expression Regulation, Plant/drug effects Gene Silencing/dru;"
Notes:"MedlineWunsche, Hendrik Baldwin, Ian T Wu, Jianqiang eng Research Support, Non-U.S. Gov't England 2011/05/31 J Exp Bot. 2011 Aug; 62(13):4605-16. doi: 10.1093/jxb/err171. Epub 2011 May 27"

 
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