Project/Area Number |
11306006
|
Research Category |
Grant-in-Aid for Scientific Research (A)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Plant nutrition/Soil science
|
Research Institution | OKAYAMA UNIVERSITY |
Principal Investigator |
MATSUMOTO Hideaki Res. Inst. For Bioresources, Okayama Univ., Professor, 資源生物科学研究所, 教授 (80026418)
|
Co-Investigator(Kenkyū-buntansha) |
EZAKI Bunichi Res. Inst. For Bioresources, Okayama Univ., Assistant Professor, 資源生物科学研究所, 助手 (90243500)
YAMAMOTO Yoko Res. Inst. For Bioresources, Okayama Univ., Associate Professor, 資源生物科学研究所, 助教授 (50166831)
|
Project Period (FY) |
1999 – 2001
|
Project Status |
Completed (Fiscal Year 2001)
|
Budget Amount *help |
¥32,880,000 (Direct Cost: ¥30,600,000、Indirect Cost: ¥2,280,000)
Fiscal Year 2001: ¥9,880,000 (Direct Cost: ¥7,600,000、Indirect Cost: ¥2,280,000)
Fiscal Year 2000: ¥11,000,000 (Direct Cost: ¥11,000,000)
Fiscal Year 1999: ¥12,000,000 (Direct Cost: ¥12,000,000)
|
Keywords | Acid soil / Aluminum stress / Aluminum tolerant gene / Malate exclusion / Transgenic rice / Aluminum injury / Mitochondrial function / Reactive oxygen species / アルミニウム / 毒性 / 耐性獲得 / 植物 / 応答反応 / 微小管 / 耐性 / 脂質過酸化 / 防御機構 / 発現タンパク質 |
Research Abstract |
The major constraint to plant growth in acid soils is the presence of toxic aluminum (Al) cations which inhibit root elongation. The enhanced Al tolerance exhibited by some cultivars of wheat is associated with the Al-dependent efflux of malate from the root apices. Malate forms a stable complex with Al which is harmless to plants, and therefore this efflux of malate forms the basis of a hypothesis to explain Al tolerance in wheat. We carried out the cloning of a wheat gene, ALMT1, that co-segregates with Al tolerance in F_2 and F_3 populations derived from crosses between near-isogenic wheat lines that differ in Al tolerance. The ALMT1 gene encodes a membrane protein that is constitutively expressed in the root apices of the AI-tolerant line at greater levels than in the near-isogenic but Al-sensitive line. Heterologous expression of ALMT1 in Xenopus oocytes, rice and cultured tobacco cells conferred an Al-activated malate efflux. Potential mechanisms of AI toxicity measured as Al-indu
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ced inhibition of growth in cultured tobacco cells (Nicotiana tabacum, nonchlorophyllic cell line SL) and pea (Pisum sativum) roots were investigated. The accumulation of Al in tobacco cells caused instantaneously the repression of mitochondrial activities and, after a lag of about 12 h, triggered reactive oxygen species (ROS) production, respiration inhibition, ATP depletion, and the loss of growth capability almost simultaneously. The presence of an antioxidant, butylated hydroxyanisol, during Al treatment of SL cells prevented not only ROS production but also ATP depletion and the loss of growth capability, suggesting that the AI-triggered ROS production seems to be a cause of ATP depletion and the loss of growth capability. Furthermore, these three late events were similarly repressed in an Al-tolerant cell line (ALT301) isolated from SL cells, suggesting that the acquisition of antioxidant functions mimicking burylated hydroxyanisol can be a mechanism of Al tolerance. We conclude that A1 affects mitochondrial functions, which leads to ROS production, probably the key critical event in Al inhibition of cell growth. Less
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