[Molecular mechanisms of plant resistance to cadmium toxicity].

Q3 Environmental Science 应用生态学报 Pub Date : 2006-06-01
Zhenghao Xu, Guojun Shen, Changqing Zhu, Linjuan Xu, Yong He, Gusong Yu
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引用次数: 0

Abstract

Cadmium (Cd) is a non-essential trace element for plants, and has strong toxicity at low concentrations. It can suppress the elongation growth of plant cell, inhibit oxidative mitochondrial phosphorylation, induce oxidative stress, inhibit the activities of several antioxidative enzymes, affect photosynthesis by inhibiting ferrous reductase or damaging photosynthesis apparatus, and cause the alteration of chromatin and the change of plasma membrane ATPase activity. In response to Cd stress, the cells of cadmium-resistant plant species can produce a number of proteins such as phytochelatins, metallothioneins and stress proteins to detoxify Cd ions, and efficiently repair Cd damage. The plant cells can also resort to other defense systems to detoxify Cd ions, e.g., the immobilization of Cd by cell wall, exclusion of Cd through the action of plasma membrane, compartmentalization of Cd by vacuolar, and release of plant glands. The phytochelatin synthase (PCS) genes of Arabidopsin, wheat and Schizosaccharomyces pombe had been identified by using different approaches, and the metallothioneins (MT) in plants was also identified recently. By introducing animal MT genes, transgenic plants could increase the resistant ability to Cd toxicity. Subjected to Cd, plant cells often start to synthesize stress proteins such as heat shock proteins, and the plants having been transformed the stress protein genes could enhance their resistant capacity to Cd ions. It was reported that zinc (Zn) ion-transporting proteins could also transport Cd ion. Some minor genes not conferring tolerance on their own could modify the major gene (s), and enhance Cd tolerance. Cd detoxification in wild type plants could be a complex phenomenon, probably under polygenic control to Cd, while acute Cd stress seemed to be a simpler mechanism, apparently involving only one or a few specific major genes.

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[植物抗镉毒性的分子机制]。
镉(Cd)是植物非必需的微量元素,在低浓度下具有很强的毒性。它可以抑制植物细胞伸长生长,抑制线粒体氧化磷酸化,诱导氧化应激,抑制几种抗氧化酶的活性,通过抑制亚铁还原酶或破坏光合作用装置影响光合作用,引起染色质的改变和质膜atp酶活性的改变。在镉胁迫下,抗镉植物细胞可产生植物螯合蛋白、金属硫蛋白和胁迫蛋白等多种蛋白质,对Cd离子进行解毒,有效修复Cd损伤。植物细胞也可以通过其他防御系统来解毒Cd离子,如细胞壁固定Cd、质膜排除Cd、液泡隔离Cd、植物腺体释放Cd等。拟南芥、小麦和裂糖菌的植物螯合素合成酶(PCS)基因已通过不同的方法进行了鉴定,近年来植物金属硫蛋白(MT)也得到了鉴定。通过引入动物MT基因,转基因植物可以提高对Cd毒性的抗性。受镉胁迫的植物细胞往往开始合成热休克蛋白等胁迫蛋白,转化了胁迫蛋白基因的植物对镉离子的抗性增强。据报道,锌离子转运蛋白也可以转运镉离子。一些不具有自身耐受性的次要基因可以修饰主要基因,从而增强对Cd的耐受性。野生型植物的Cd解毒可能是一个复杂的现象,可能受到Cd的多基因控制,而急性Cd胁迫似乎是一个更简单的机制,显然只涉及一个或几个特定的主要基因。
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来源期刊
应用生态学报
应用生态学报 Environmental Science-Ecology
CiteScore
2.50
自引率
0.00%
发文量
11393
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