title: Overexpression of dehydroascorbate reductase, but not monodehydroascorbate reductase, confers tolerance to aluminum stress in transgenic tobacco.
abstract: Aluminum (Al) inhibits plant growth partly by causing oxidative damage that is promoted by reactive oxygen species and can be prevented by improving antioxidant capacity. Ascorbic acid (AsA), the most abundant antioxidant in plants, is regenerated by the action of monodehydroascorbate reductase (MDAR) and dehydroascorbate reductase (DHAR). We investigated the role of MDAR and DHAR in AsA regeneration during Al stress using transgenic tobacco (Nicotiana tabacum) plants overexpressing Arabidopsis cytosolic MDAR (MDAR-OX) or DHAR (DHAR-OX). DHAR-OX plants showed better root growth than wild-type (SR-1) plants after exposure to Al for 2 weeks, but MDAR-OX plants did not. There was no difference in Al distribution and accumulation in the root tips among SR-1, DHAR-OX, and MDAR-OX plants after Al treatment for 24 h. However, DHAR-OX plants showed lower hydrogen peroxide content, less lipid peroxidation and lower level of oxidative DNA damage than SR-1 plants, whereas MDAR-OX plants showed the same extent of damage as SR-1 plants. Compared with SR-1 plants, DHAR-OX plants consistently maintained a higher AsA level both with and without Al exposure, while MDAR-OX plants maintained a higher AsA level only without Al exposure. Also, DHAR-OX plants maintained higher APX activity under Al stress. The higher AsA level and APX activity in DHAR-OX plants contributed to their higher antioxidant capacity and higher tolerance to Al stress. These findings show that the overexpression of DHAR, but not of MDAR, confers Al tolerance, and that maintenance of a high AsA level is important to Al tolerance.
authors: Laboratory of Plant Biotechnology, The United Graduate School of Agricultural Sciences, Tottori University, Koyama, Minami 4-101, Tottori 680-8553, Japan. linayincau@yahoo.co.jp
authors: Lina
authors: L
authors: Yin
authors: Shiwen
authors: S
authors: Wang
authors: Amin Elsadig
authors: AE
authors: Eltayeb
authors: Md Imtiaz
authors: MI
authors: Uddin
authors: Yoko
authors: Y
authors: Yamamoto
authors: Wataru
authors: W
authors: Tsuji
authors: Yuichi
authors: Y
authors: Takeuchi
authors: Kiyoshi
authors: K
authors: Tanaka
mesh_terms: D000535:Aluminum / Q000633:toxicity*; D017360:Arabidopsis / Q000235:genetics; D001205:Ascorbic Acid / Q000378:metabolism; D004249:DNA Damage; D005978:Glutathione / Q000378:metabolism; D006861:Hydrogen Peroxide / Q000378:metabolism; D015227:Lipid Peroxidation / Q000187:drug effects; D009247:NADH, NADPH Oxidoreductases / Q000235:genetics* / Q000378:metabolism / Q000502:physiology; D018384:Oxidative Stress; D010088:Oxidoreductases / Q000235:genetics* / Q000378:metabolism / Q000502:physiology; D010940:Plant Proteins / Q000235:genetics* / Q000378:metabolism / Q000502:physiology; D018517:Plant Roots / Q000187:drug effects / Q000235:genetics / Q000254:growth & development / Q000378:metabolism; D030821:Plants, Genetically Modified / Q000187:drug effects* / Q000201:enzymology / Q000254:growth & development; D014026:Nicotiana / Q000187:drug effects / Q000201:enzymology / Q000235:genetics*
chemical_list: D010940:Plant Proteins; D006861:Hydrogen Peroxide; D000535:Aluminum; D010088:Oxidoreductases; D009247:NADH, NADPH Oxidoreductases; C023927:monodehydroascorbate reductase (NADH); C020666:glutathione dehydrogenase (ascorbate); D005978:Glutathione; D001205:Ascorbic Acid