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The genetics of plant oxidative stress tolerance. Overmyer, Kirk1, 1 Biology Department, Chapel Hill, NC, USA ABSTRACT- Genetically tractable model systems such as Arabidopsis make possible the dissection of oxidative stress responses at the molecular level. Reverse genetic approaches have further defined the roles of antioxidants and stress hormones. Forward genetic screens allow the opening of new avenues of research, as illustrated by the radical induced cell death1 (rcd1) mutant, which was isolated based on its ozone sensitivity. The rcd1 mutant is differentially sensitive to reactive oxygen species (ROS) depending on the species and its site of generation. Specifically, rcd1 cell death is triggered by ozone, apoplastic superoxide but not by hydrogen peroxide or paraquat. In fact, compared to wildtype, rcd1 is paraquat tolerant. In addition to higher initial levels of ROS-induced cell death rcd1 exhibits transient superoxide-dependent spreading cell death. To explore the role of various ROS sources, double mutants were made with knockouts of the Atrboh (Arabidopsis respiratory burst oxidase homolog) genes, which encode NADPH oxidase subunits involved in production of the plant oxidative burst. ROS accumulation and cell death were both reduced in rcd1 atrbohD, while ROS accumulation was unchanged and cell death enhanced in rcd1 atrbohF. Beyond its ROS sensitivity, rcd1 exhibits reduced sensitivity to multiple stress hormones as well as developmental changes. Map based cloning revealed that RCD1 belongs to the (ADP-ribosyl)transferase domain containing subfamily of the WWE-domain protein family and is putatively involved in the covalent modification of target proteins by the addition of ADPribose units. The WWE domain is a globular protein-protein interaction platform, which may be involved in substrate recruitment. Key words: Oxidative stress, Arabidopsis thaliana, mutants, ozone |
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