Nitric Oxide and Protein S-Nitrosylation Are Integral Hydrogen Peroxide-Induced Leaf Cell Death in Rice1[W][OA].

Nitric oxide (NO) is a key redox-active, small molecule involved in various aspects of plant growth and development. Here, we report the identification of an NO accumulation mutant, nitric oxide excess1 (noe1), in rice (Oryza sativa), the isolation of the corresponding gene, and the analysis of its role in NO-mediated leaf cell death. Map-based cloning revealed that NOE1 encoded a rice catalase, OsCATC. Furthermore, noel resulted in an increase of hydrogen peroxide (H₂O₂) in the leaves, which consequently promoted NO production via the activation of nitrate reductase. The removal of excess NO reduced cell death in both leaves and suspension cultures derived from noel plants, implicating NO as an important endogenous mediator of H₂O₂-induced leaf cell death. Reduction of intracellular S-nitrosothiol (SNO) levels, generated by overexpression office S-nitrosoglutathione reductase gene (GSNOR1), which regulates global levels of protein S-nitrosylation, alleviated leaf cell death in noel plants. Thus, S-nitrosylation was also involved in light-dependent leaf cell death in noel. Utilizing the bio in-switch assay, nanoliquid chromatography and tandem mass spectrometry S-nitrosylated proteins were identified in both wild-type and noel plants. NO targets identified only in noel plants included glyceraldehyde 3-phosphate dehydrogenase and that oredoxin, which have been reported to be involved in S-nitrosylation-regulated cell death in animals. Collectively our data suggest that both NO and SNOs are important mediators in the process of H₂O₂-induced leaf cell death in rice. [ABSTRACT FROM AUTHOR]