酸性土壤上植物应对铝胁迫的过程与机制

铝胁迫是酸性土壤上影响作物产量最重要的因素之一.目前,全球土壤酸化程度进一步加剧了铝胁迫.植物可通过将铝离子与有机酸螯合储藏于液泡和从根系中排出铝毒.排出铝毒主要通过苹果酸转运蛋白ALMT和柠檬酸转运蛋白MATE的跨膜运输来实现.编码ABC转运蛋白和锌指转录因子的基因与植物抗铝胁迫有关.这些抗铝毒基因的鉴别使得通过转基因和分子标记辅助育种等生物技术来提高农作物的抗铝毒能力成为可能.最后提出了植物抗铝胁迫研究中需要解决的关键问题及今后的研究方向.     

丹波黑大豆GmbHLH30转录因子耐铝功能初步研究

铝毒是酸性土壤作物生长的主要限制因素。前期研究发现,铝胁迫下,耐铝型丹波黑大豆SSH(suppression subtractive hybridization,SSH)cDNA文库中bHLH30转录因子基因上调表达,推测该基因与丹波黑大豆耐铝性相关。克隆GmbHLH30基因,构建GmbHLH30植物表达载体pK2-35S-GmbHLH30,并在烟草中过量表达获得转GmbHLH30的转基因烟草植株。在铝胁迫下,转GmbHLH30的转基因烟草相对根伸长率比野生型烟草大,可溶性糖和脯氨酸含量高,H2O2水平低。表明GmbHLH30基因的过量表达可以增强植物的耐铝能力,暗示GmbHLH30转录因子参与调控植物的耐铝特性。     

植物适应酸铝胁迫机理的研究进展

酸铝胁迫是限制植物正常生长发育的重要非生物胁迫因子,严重制约了我国酸性土壤地区的农业生产水平。植物抵御酸铝胁迫的形式复杂多样,如分泌有机酸、提高根际pH、分泌黏液、细胞壁对Al³⁺的固定、有机酸对细胞溶质中Al³⁺的螯合与液泡区隔化等。现有研究多集中于常规生理特征分析,缺乏深入的分子生物学解析。基于此,本文对国内外植物适应酸铝胁迫机理的相关研究进行了归纳和总结,从酸铝胁迫对植物生长与生理代谢的影响、植物适应酸铝胁迫最主要的两种生理机制(Al排除机制、Al耐受机制)以及分子水平上调控相关耐铝基因进行了综述。最后针对现有研究的不足提出了展望,以期为深入揭示植物适应酸铝胁迫的机理以及挖掘适于酸土生长的优质作物资源提供理论依据。     

植物耐铝的生物化学与分子机理

某些耐铝植物在铝胁迫下分泌有机酸被认为是一个重要的抗性机制.从根系分泌出来的有机酸能与根际的Al3 结合,形成无毒性的螯合物,从而减轻了铝对根系的毒害.但是,铝诱导有机酸分泌的中间环节及调节机制至今仍不清楚.一些证据表明,铝能激活根尖细胞质膜内的阴离子通道,因而可以调节有机酸的分泌.近年来,人们开始注意一些信号分子如蛋白激酶、水杨酸等介导铝诱导有机酸的分泌,已经获得一些成果.同时,铝胁迫基因的分离和鉴定也为人们从分子水平上研究和认识铝胁迫下植物的抗性机制奠定了基础.     

植物铝离子胁迫的研究方法综述

酸性土壤上,植物的生长受到很大的抑制,铝对植物的毒害是最主要的问题。为了揭示植物铝离子胁迫反应及其耐铝性的机理,科学家们进行了大量研究,取得了许多喜人的进展。根据前人研究,对植物铝离子胁迫的研究方法进行了综述。在试验材料的处理方面介绍了大田栽培、室外盆栽、室内盆栽、营养液栽培等方法;在耐铝性鉴定方面介绍了受害症状、根相对伸长率等直接鉴定法和化学染色、有机酸分泌量等间接鉴定法;在铝离子胁迫基因研究方面,介绍了基因定位技术、基因差异表达研究技术、蛋白质差异表达研究技术及转基因技术等研究方法。     

生长素及其运输蛋白对植物铝胁迫的响应

铝对植物的毒害作用主要表现为抑制根尖生长,而根尖生长与生长素及其运输密切相关,铝可能影响了生长素及其代谢过程,但目前尚不清楚生长素及其运输蛋白如何参与植物应对铝胁迫响应。本文通过分析、总结前人研究,并结合自己的前期研究结果,初步阐述生长素或其运输蛋白对植物铝胁迫的响应,即铝影响生长素代谢的相关基因,干扰根尖生长素运输蛋白在细胞内分布及其囊泡运输,调控生长素的极性运榆,进而抑制根尖生长。另一方面,生长素或其运输蛋白又参与了植物应对铝胁迫过程,这主要体现在参与了植物铝毒信号传递、根系铝内置化过程和减缓铝诱导的氧化胁迫。最后,本文提出了生长素及其运输蛋白对植物铝胁迫响应的可能模型。     

铝诱导植物程序性细胞死亡信号转导的研究进展

铝是制约酸性土壤上作物生产的主要因素。铝诱导氧化胁迫产生大量活性氧/一氧化氮,引起胞质钙超载,通过线粒体信号转导途径激发相关凋亡基因,从而引起细胞主动死亡,以减轻铝对植物的进一步毒害。本文综述了铝诱导程序性细胞死亡的信号分子、相关基因以及信号转导途径,对未来的研究方向提出了展望,为深入研究植物铝毒害机理和耐铝机制提供参考。     

铝胁迫下植物根系的有机酸分泌及其解毒机理

酸性土壤中的铝毒害问题,已成为限制植物生长发育的主要因素之一.耐铝植物通过根系分泌有机酸来解除或减轻铝的毒害是外部解铝毒的重要机制.文章对铝胁迫下植物根系分泌有机酸的种类,有机酸解铝毒机理、解铝毒能力,有机酸分泌方式及调控其分泌的主要因素等相关研究进行综述.     

光学无损分析技术在植物铝毒性研究中的应用

光学技术以它所特有的无损、快速和在位分析的优势,广泛应用于植物逆境生理监测和逆境胁迫机制研究.作为一类最主要的逆境胁迫,铝毒性是酸性土壤限制作物生长的主要原因.本文从光学分子成像和在位实时监测两个功能层面上概述了光学分析技术在铝毒生物学机制研究和铝毒性生理探测中的应用,并对其做了展望,同时,也讨论了铝毒性生物胁迫机制尚未涉及的问题,以期为铝胁迫机制研究提供有用的技术和理论参考.     

植物适应铝毒胁迫的生理及分子生物学机理

铝毒是酸性土壤上限制作物生长最重要的因素,严重影响着全世界和中国大约40％和21％耕作土壤的作物生产．近几十年来,世界各国针对植物的铝毒及其耐铝机制进行了大量的研究,并取得了较大进展．文中重点综述了植物适应铝胁迫基因型差异筛选方法及其鉴定技术、植物适应铝胁迫的生理基础及分子生物学机制等方面的研究进展,简要讨论了今后的研究方向．     

Expression of aluminum-induced genes in transgenic arabidopsis plants can ameliorate aluminum stress and/or oxidative stress

To examine the biological role of Al-stress-induced genes, nine genes derived from Arabidopsis, tobacco (Nicotiana tabacum L.), wheat (Triticum aestivum L.), and yeast (Saccharomyces cerevisiae) were expressed in Arabidopsis ecotype Landsberg. Lines containing eight of these genes were phenotypically normal and were tested in root elongation assays for their sensitivity to Al, Cd, Cu, Na, Zn, and to oxidative stresses. An Arabidopsis blue-copper-binding protein gene (AtBCB), a tobacco glutathione S-transferase gene (parB), a tobacco peroxidase gene (NtPox), and a tobacco GDP-dissociation inhibitor gene (NtGDI1) conferred a degree of resistance to Al. Two of these genes, AtBCB and parB, and a peroxidase gene from Arabidopsis (AtPox) also showed increased resistance to oxidative stress induced by diamide, while parB conferred resistance to Cu and Na. Al content of Al-treated root tips was reduced in the four Al-resistant plant lines compared with wild-type Ler-0, as judged by morin staining. All four Al-resistant lines also showed reduced staining of roots with 2',7'-dichloro fluorescein diacetate (H(2)DCFDA), an indicator of oxidative stress. We conclude that Al-induced genes can serve to protect against Al toxicity, and also provide genetic evidence for a link between Al stress and oxidative stress in plants.     

AHA1转基因拟南芥的抗铝性生理解析

AHA1基因是植物体内编码质膜H⁺ATPase的一个重要基因,参与植物的生长发育与抗逆胁迫反应.本文以AHA1转基因型及其野生型拟南芥为材料,研究了铝胁迫对拟南芥养分吸收、抗氧化胁迫和有机酸分泌的影响.结果表明：Al降低了拟南芥根系对N、K、Ca和Mg的吸收,但增加了根系对P的吸收,且AHA1转基因型拟南芥比野生型积累更多的P和较少的Al.铝胁迫诱导拟南芥抗氧化酶SOD和POD活性增加,转基因型与野生型之间没有明显差异.Al对拟南芥有机酸分泌具有明显的诱导作用,且AHA1转基因型分泌较多的有机酸.质膜H⁺ATPase的活性抑制剂钒酸盐对拟南芥有机酸分泌具有明显的抑制作用;而Zn²⁺、Mg²⁺可促进Al对拟南芥有机酸分泌的诱导,并部分恢复钒酸盐的抑制效应.说明AHA1基因通过增加拟南芥根系对P的吸收以及有机酸分泌,提高了植物的抗铝性.     

Aluminium-induced drought and oxidative stress in barley roots

The aim of the present study was to examine the relation between Al accumulation in root tissues, root growth inhibition, root water content, cell viability and expression of oxidative and drought stress-related genes in barley roots growing on the filter paper. Al-induced root growth inhibition correlated with Al uptake and cell death. Water content of Al-treated root represented only half of the control one. The expression of the dehydrin gene dhn4, which is a marker for drought stress in plant tissues, was strongly induced during Al stress. Al treatment also induced expression of oxidative stress-related genes such as glutathione peroxidase (gpx), pathogen-related peroxidase (prx8), glutathione reductase (gr) and dehydroascorbate reductase (dhar). The present results suggest correlation between Al uptake, Al-induced drought stress, oxidative stress, cell death and root growth inhibition.     

Recent progress in the research of external Al detoxification in higher plants: a minireview

Aluminum (Al) is highly toxic to plant growth. The toxicity is characterized by rapid inhibition of root elongation. However, some plant species and cultivars have evolved some mechanisms for detoxifying Al both internally and externally. In this review, the recent progress made in the research of external detoxification of Al is described. Accumulating evidence has shown that organic acids play an important role in the detoxification of Al. Some plant species and cultivars respond to Al by secreting citrate, malate or oxalate from the roots. Recently, the anion channel of malate and citrate in the plasma membrane has been characterized and a gene encoding the malate channel has been cloned. The metabolism of organic acids seems to be poorly correlated with the Al-induced secretion of organic acid anions. A number of QTLs (quantitative trait loci) for Al resistance have been identified in rice, Arabidopsis, and other species. Transgenic plants with enhanced resistance to Al have also been reported, but introduction of multiple genes may be required to gain high Al resistance in future.     

The Physiology, Genetics and Molecular Biology of Plant Aluminum Resistance and Toxicity

Aluminum (Al) toxicity is the primary factor limiting crop production on acidic soils (pH values of 5 or below), and because 50% of the world’s potentially arable lands are acidic, Al toxicity is a very important limitation to worldwide crop production. This review examines our current understanding of mechanisms of Al toxicity, as well as the physiological, genetic and molecular basis for Al resistance. Al resistance can be achieved by mechanisms that facilitate Al exclusion from the root apex (Al exclusion) and/or by mechanisms that confer the ability of plants to tolerate Al in the plant symplasm (Al tolerance). Compelling evidence has been presented in the literature for a resistance mechanism based on exclusion of Al due to Al-activated carboxylate release from the growing root tip. More recently, researchers have provided support for an additional Al-resistance mechanism involving internal detoxification of Al with carboxylate ligands (deprotonated organic acids) and the sequestration of the Al-carboxylate complexes in the vacuole. This is a field that is entering a phase of new discovery, as researchers are on the verge of identifying some of the genes that contribute to Al resistance in plants. The identification and characterization of Al resistance genes will not only greatly advance our understanding of Al-resistance mechanisms, but more importantly, will be the source of new molecular resources that researchers will use to develop improved crops better suited for cultivation on acid soils.