title: Nitric oxide activates superoxide dismutase and ascorbate peroxidase to repress the cell death induced by wounding.
abstract: Wounding caused by rain, wind, and pathogen may lead plants to onset defense response. Previous studies indicated that mechanical wounding stimulates plants to generate nitric oxide (NO) and hydrogen peroxide (H(2)O(2)). In this study, the functions of NO and H(2)O(2) after wounding in sweet potato (Ipomoea batatas cv. Tainung 57) was further analyzed. Mechanical wounding damaged cells and resulted in necrosis, but the presence of NO donors or NO scavenger might reduce or enhance the cell death caused by wounding, respectively. The amount of H(2)O(2) induced by wounding was also decreased or increased when plants were incubated with NO donors or NO scavenger, individually. These results indicate that NO may regulate H(2)O(2) generation to affect cell death. NO-induced proteins isolated from two-dimensional electrophoresis were identified to be Copper/Zinc superoxide dismutases (CuZnSODs). The activities of CuZnSODs and ascorbate peroxidase (APX) could be enhanced by NO. In addition, the expression of CuZnSOD and APX was induced by wounding via NO, and their expression was further stimulated by NO through the generation of cGMP. The influx of calcium ions and the activity of NADPH oxidase were also involved in the NO signal transduction pathway inducing APX expression. Collectively, the generation of H(2)O(2) in wounded plants might trigger cell death. Meanwhile, the production of NO induced by wounding stimulated signal transducers including cGMP, calcium ions, and H(2)O(2) to activate CuZnSOD and APX, which further decreased H(2)O(2) level and reduced the cell death caused by wounding.
authors.affiliation: Institute of Plant Biology, National Taiwan University, Taipei 106, Taiwan, Republic of China. f92b42009@ntu.edu.tw
authors.forename: Chih-Ching
authors.initials: CC
authors.lastname: Lin
authors.forename: Pei-Ju
authors.initials: PJ
authors.lastname: Jih
authors.forename: Hsin-Hung
authors.initials: HH
authors.lastname: Lin
authors.forename: Jeng-Shane
authors.initials: JS
authors.lastname: Lin
authors.forename: Ling-Lan
authors.initials: LL
authors.lastname: Chang
authors.forename: Yu-Hsing
authors.initials: YH
authors.lastname: Shen
authors.forename: Shih-Tong
authors.initials: ST
authors.lastname: Jeng
mesh_terms: D060387:Ascorbate Peroxidases / Q000235:genetics / Q000378:metabolism*; D001565:Benzoates / Q000494:pharmacology; D015152:Blotting, Northern; D016923:Cell Death / Q000187:drug effects; D006152:Cyclic GMP / Q000378:metabolism; D015180:Electrophoresis, Gel, Two-Dimensional; D004789:Enzyme Activation / Q000187:drug effects; D015971:Gene Expression Regulation, Enzymologic / Q000187:drug effects; D018506:Gene Expression Regulation, Plant / Q000187:drug effects; D006861:Hydrogen Peroxide / Q000378:metabolism; D007093:Imidazoles / Q000494:pharmacology; D027723:Ipomoea batatas / Q000201:enzymology / Q000235:genetics / Q000378:metabolism; D009569:Nitric Oxide / Q000037:antagonists & inhibitors / Q000378:metabolism*; D020030:Nitric Oxide Donors / Q000378:metabolism / Q000494:pharmacology*; D009599:Nitroprusside / Q000378:metabolism / Q000494:pharmacology; D020133:Reverse Transcriptase Polymerase Chain Reaction; D026423:S-Nitroso-N-Acetylpenicillamine / Q000494:pharmacology; D013314:Stress, Mechanical; D013482:Superoxide Dismutase / Q000235:genetics / Q000378:metabolism*
chemical_list: D001565:Benzoates; D007093:Imidazoles; D020030:Nitric Oxide Donors; C079393:1,3-dihydroxy-4,4,5,5-tetramethyl-2-(4-carboxyphenyl)tetrahydroimidazole; D009599:Nitroprusside; D009569:Nitric Oxide; D026423:S-Nitroso-N-Acetylpenicillamine; D006861:Hydrogen Peroxide; D060387:Ascorbate Peroxidases; D013482:Superoxide Dismutase; D006152:Cyclic GMP