Research on the plant response to A1 stress and the production of Al tolerant plant

在酸性土壤中，植物生长的主要制约因素是有毒的铝（Al）阳离子的存在，这抑制了根系的伸长。一些小麦品种对铝的耐受性增强与苹果酸从根尖流出铝有关。苹果酸盐与铝形成稳定的复合物，对植物无害，因此苹果酸盐的外排形成了解释小麦耐铝性假设的基础。在铝耐受性不同的近等基因小麦系的F_2和F_3群体中，克隆了一个与铝耐受性共分离的小麦基因ALMT1。ALMT1基因编码一种膜蛋白，该膜蛋白在耐ai品系的根尖上的表达水平高于接近等基因的铝敏感品系。在非洲爪蟾卵母细胞、水稻和培养的烟草细胞中，ALMT1的异源表达赋予了al激活的苹果酸外排。研究了AI对培养的烟草细胞（Nicotiana tabacum， non -叶绿素细胞系SL）和豌豆（Pisum sativum）根系生长的抑制作用。Al在烟草细胞中的积累立即引起线粒体活性的抑制，滞后约12 h后，几乎同时引发活性氧（ROS）的产生、呼吸抑制、ATP消耗和生长能力的丧失。在Al处理SL细胞的过程中，抗氧化剂丁基羟基异醇的存在不仅阻止了ROS的产生，还阻止了ATP的消耗和生长能力的丧失，这表明ai触发的ROS的产生似乎是ATP消耗和生长能力丧失的原因。此外，这三个后期事件在从SL细胞分离出来的耐铝细胞系（ALT301）中也同样受到抑制，这表明获得类似于burylated羟基异醇的抗氧化功能可能是铝耐受性的一种机制。我们得出结论，A1影响线粒体功能，从而导致ROS的产生，这可能是Al抑制细胞生长的关键事件。少

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 … More 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