Overaccumulation of γ-Glutamylcysteine in a Jasmonate-Hypersensitive Arabidopsis Mutant Causes Jasmonate-Dependent Growth Inhibition  . Issue 2 (17th August 2015)

• Record Type: Journal Article
• Authors: Wei, Hsin-Ho; Rowe, Martha; Riethoven, Jean-Jack M.; Grove, Ryan; Adamec, Jiri; Jikumaru, Yusuke; Staswick, Paul
• Is Part Of: Plant physiology. Volume 169:Issue 2(2015)
• Page Start: 1371
• Page End: 1381
• Publication Date: 2015-08-17
• Subjects: Plant physiology -- Periodicals; Botany -- Periodicals; Periodicals; Electronic journals; 571.2
• DOI: 10.1104/pp.15.00999
• Languages: English
• ISSNs: 0032-0889

Abstract

Abstract : The glutathione precursor γ-glutamylcysteine modulates plant growth inhibition by the jasmonate hormone. Abstract: Glutathione (GSH ) is essential for many aspects of plant biology and is associated with jasmonate signaling in stress responses. We characterized an Arabidopsis ( Arabidopsis thaliana ) jasmonate-hypersensitive mutant ( jah2 ) with seedling root growth 100-fold more sensitive to inhibition by the hormone jasmonyl-isoleucine than the wild type. Genetic mapping and genome sequencing determined that the mutation is in intron 6 of GLUTATHIONE SYNTHETASE2, encoding the enzyme that converts γ-glutamylcysteine (γ-EC ) to GSH . The level of GSH in jah2 was 71% of the wild type, while the phytoalexin-deficient2-1 ( pad2-1 ) mutant, defective in GSH1 and having only 27% of wild-type GSH level, was not jasmonate hypersensitive. Growth defects for jah2, but not pad2, were also seen in plants grown to maturity. Surprisingly, all phenotypes in the jah2 pad2-1 double mutant were weaker than in jah2 . Quantification of γ-EC indicated these defects result from hyperaccumulation of this GSH precursor by 294- and 65-fold in jah2 and the double mutant, respectively. γ-EC reportedly partially substitutes for loss of GSH, but growth inhibition seen here was likely not due to an excess of total glutathione plus γ-EC because their sum in jah2 pad2-1 was only 16% greater than in the wild type. Further, the jah2 phenotypes were lost in a jasmonic acid biosynthesis mutant background, indicating the effect of γ-EC is mediated through jasmonate signaling and not as a direct result of perturbed redox status.