Overaccumulation ofγ-Glutamylcysteine in a Jasmonate-Hypersensitive Arabidopsis Mutant Causes Jasmonate-Dependent Growth Inhibition

• Published in: Plant physiology (Bethesda) Vol. 169; no. 2; pp. 1371 - 1381
• Main Authors: Wei, Hsin-Ho, Rowe, Martha, Riethoven, Jean-Jack M., Grove, Ryan, Adamec, Jiri, Jikumaru, Yusuke, Staswick, Paul
• Format: Journal Article
• Language: English
• Published: United States American Society of Plant Biologists 01.10.2015
• Subjects: Arabidopsis - drug effects; Arabidopsis - genetics; Arabidopsis - growth & development; Arabidopsis - metabolism; Arabidopsis Proteins - genetics; Arabidopsis Proteins - metabolism; Biology; Complementary DNA; Cyclopentanes - metabolism; Cyclopentanes - pharmacology; Dipeptides - metabolism; Gene Expression Regulation, Plant - drug effects; Glutathione - metabolism; Glutathione Synthase - genetics; Glutathione Synthase - metabolism; Hypersensitivity; Introns; Mutation; Oxylipins - metabolism; Oxylipins - pharmacology; Phenotypes; Plant growth; Plant roots; Plant Roots - genetics; Plant Roots - growth & development; Plant Roots - metabolism; Plants; Plants, Genetically Modified; Root growth; Seedlings; Seedlings - genetics; Seedlings - growth & development; Seedlings - metabolism; SIGNALING AND RESPONSE
• ISSN: 0032-0889; 1532-2548
• DOI: 10.1104/pp.15.00999

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 ofGLUTATHIONE SYNTHETASE2, encoding the enzyme that convertsγ-glutamylcysteine (γ-EC) to GSH. The level of GSH injah2was 71% of the wild type, while thephytoalexin-deficient2-1(pad2-1) mutant, defective inGSH1and having only 27% of wild-type GSH level, was not jasmonate hypersensitive. Growth defects forjah2, but notpad2, were also seen in plants grown to maturity. Surprisingly, all phenotypes in thejah2 pad2-1double mutant were weaker than injah2. Quantification ofγ-EC indicated these defects result from hyperaccumulation of this GSH precursor by 294- and 65-fold injah2and 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 plusγ-EC because their sum injah2 pad2-1was only 16% greater than in the wild type. Further, thejah2phenotypes were lost in a jasmonic acid biosynthesis mutant background, indicating the effect ofγ-EC is mediated through jasmonate signaling and not as a direct result of perturbed redox status.