SummaryThe 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 ef¯ux of malate from root apices. Malate forms a stable complex with Al that is harmless to plants and, therefore, this ef¯ux of malate forms the basis of a hypothesis to explain Al tolerance in wheat. Here, we report on the cloning of a wheat gene, ALMT1 (aluminum-activated malate transporter), 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, which is constitutively expressed in the root apices of the Al-tolerant line at greater levels than in the near-isogenic but Alsensitive line. Heterologous expression of ALMT1 in Xenopus oocytes, rice and cultured tobacco cells conferred an Al-activated malate ef¯ux. Additionally, ALMT1 increased the tolerance of tobacco cells to Al treatment. These ®ndings demonstrate that ALMT1 encodes an Al-activated malate transporter that is capable of conferring Al tolerance to plant cells.
Aluminum (Al) tolerance in Arabidopsis is a genetically complex trait, yet it is mediated by a single physiological mechanism based on Al-activated root malate efflux. We investigated a possible molecular determinant for Al tolerance involving a homolog of the wheat Al-activated malate transporter, ALMT1. This gene, named AtALMT1 (At1g08430), was the best candidate from the 14-member AtALMT family to be involved with Al tolerance based on expression patterns and genomic location. Physiological analysis of a transferred DNA knockout mutant for AtALMT1 as well as electrophysiological examination of the protein expressed in Xenopus oocytes showed that AtALMT1 is critical for Arabidopsis Al tolerance and encodes the Al-activated root malate efflux transporter associated with tolerance. However, gene expression and sequence analysis of AtALMT1 alleles from tolerant Columbia (Col), sensitive Landsberg erecta (Ler), and other ecotypes that varied in Al tolerance suggested that variation observed at AtALMT1 is not correlated with the differences observed in Al tolerance among these ecotypes. Genetic complementation experiments indicated that the Ler allele of AtALMT1 is equally effective as the Col allele in conferring Al tolerance and Al-activated malate release. Finally, fine-scale mapping of a quantitative trait locus (QTL) for Al tolerance on chromosome 1 indicated that AtALMT1 is located proximal to this QTL. These results indicate that AtALMT1 is an essential factor for Al tolerance in Arabidopsis but does not represent the major Al tolerance QTL also found on chromosome 1. abiotic stress ͉ electrophysiology ͉ genetics ͉ organic acid exudation
Pea (Pisum sativum) roots were treated with aluminum in a calcium solution, and lipid peroxidation was investigated histochemically and biochemically, as well as other events caused by aluminum exposure. Histochemical stainings were observed to distribute similarly on the entire surface of the root apex for three events (aluminum accumulation, lipid peroxidation, and callose production), but the loss of plasma membrane integrity (detected by Evans blue uptake) was localized exclusively at the periphery of the cracks on the surface of root apex. The enhancement of four events (aluminum accumulation, lipid peroxidation, callose production, and root elongation inhibition) displayed similar aluminum dose dependencies and occurred by 4 h. The loss of membrane integrity, however, was enhanced at lower aluminum concentrations and after longer aluminum exposure (8 h). The addition of butylated hydroxyanisole (a lipophilic antioxidant) during aluminum treatment completely prevented lipid peroxidation and callose production by 40%, but did not prevent or slow the other events. Thus lipid peroxidation is a relatively early symptom induced by the accumulation of aluminum and appears to cause, in part, callose production, but not the root elongation inhibition; by comparison, the loss of plasma membrane integrity is a relatively late symptom caused by cracks in the root due to the inhibition of root elongation.
Acid soils restrict plant production around the world. One of the major limitations to plant growth on acid soils is the prevalence of soluble aluminium (Al(3+)) ions which can inhibit root growth at micromolar concentrations. Species that show a natural resistance to Al(3+) toxicity perform better on acid soils. Our understanding of the physiology of Al(3+) resistance in important crop plants has increased greatly over the past 20 years, largely due to the application of genetics and molecular biology. Fourteen genes from seven different species are known to contribute to Al(3+) tolerance and resistance and several additional candidates have been identified. Some of these genes account for genotypic variation within species and others do not. One mechanism of resistance which has now been identified in a range of species relies on the efflux of organic anions such as malate and citrate from roots. The genes controlling this trait are members of the ALMT and MATE families which encode membrane proteins that facilitate organic anion efflux across the plasma membrane. Identification of these and other resistance genes provides opportunities for enhancing the Al(3+) resistance of plants by marker-assisted breeding and through biotechnology. Most attempts to enhance Al(3+) resistance in plants with genetic engineering have targeted genes that are induced by Al(3+) stress or that are likely to increase organic anion efflux. In the latter case, studies have either enhanced organic anion synthesis or increased organic anion transport across the plasma membrane. Recent developments in this area are summarized and the structure-function of the TaALMT1 protein from wheat is discussed.
Acidity is a serious limitation to plant production on many of the world's agricultural soils. Toxic aluminium (Al) cations solubilized by the acidity rapidly inhibit root growth and limit subsequent uptake of water and nutrients. Recent work has shown that the ALMT1 gene of wheat (Triticum aestivum) encodes a malate transporter that is associated with malate efflux and Al tolerance. We generated transgenic barley (Hordeum vulgare) plants expressing ALMT1 and assessed their ability to exude malate and withstand Al stress. ALMT1 expression in barley conferred an Al-activated efflux of malate with properties similar to those of Al-tolerant wheat. The transgenic barley showed a high level of Al tolerance when grown in both hydroponic culture and on acid soils. These findings provide additional evidence that ALMT1 is a major Al-tolerance gene and demonstrate its ability to confer effective tolerance to acid soils through a transgenic approach in an important crop species.A cid soils cover some 40% of the Earth's arable land and represent a major limitation to plant production (1). The main constraint to plant growth on these soils is the aluminum (Al) that is solubilized by the acidity into the toxic Al 3ϩ cation. Al toxicity is manifest by inhibition of root growth resulting in poor uptake of water and nutrients (2). Plant production on acid soils can be maintained by neutralizing the acidity with lime (CaCO 3 ) and through the use of Al-tolerant plant species. Lime can take decades to correct acidity at depth, and many important crop and pasture species lack sufficient Al tolerance within their germplasm to allow effective breeding for this character. Genetic engineering provides an opportunity to enhance the Al tolerance of sensitive species through the overexpression of endogenous genes or by the expression of foreign genes. Toward this end, the Al tolerance of canola (Brassica napus) (3), Arabidopsis thaliana (4), tobacco (Nicotiana tabacum) (5), and alfalfa (Medicago sativum) (6) have been reported to be enhanced by increasing organic acid biosynthesis through overexpression of citrate synthase or malate dehydrogenase genes derived from plants or bacteria. Other strategies have sought to increase Al tolerance by overexpression of genes associated with stress responses (7-9). In some cases, manipulation of organic acid biosynthesis has led to increased secretion of organic acids from roots, and the increased Al tolerance was attributed to the ability of organic acids to chelate and detoxify Al 3ϩ . However, the increases in Al tolerance have at best been modest or, as in the case of a Psuedomonas aeuriginosa citrate synthase gene, not easily reproducible (10). Whereas an enhanced ability to secrete organic acids from roots might need to be linked to the biosynthesis of organic acids, the transport of these molecules to the external medium appears to be a rate-limiting step (11).The Al-activated efflux of organic acid anions from roots is now a well established mechanism that is proposed to be used by a range of...
Plant stomata limit both carbon dioxide uptake and water loss; hence, stomatal aperture is carefully set as the environment fluctuates. Aperture area is known to be regulated in part by ion transport, but few of the transporters have been characterized. Here we report that AtALMT12 (At4g17970), a homolog of the aluminum-activated malate transporter (ALMT) of wheat, is expressed in guard cells of Arabidopsis thaliana. Loss-of-function mutations in AtALMT12 impair stomatal closure induced by ABA, calcium and darkness, but do not abolish either the rapidly activated or the slowly activated anion currents previously identified as being important for stomatal closure. Expressed in Xenopus oocytes, AtALMT12 facilitates chloride and nitrate currents, but not those of organic solutes. Therefore, we conclude that AtALMT12 is a novel class of anion transporter involved in stomatal closure.
Potential mechanisms of Al toxicity measured as Al-induced inhibition of growth in cultured tobacco cells (Nicotiana tabacum, nonchlorophyllic cell line SL) and pea (Pisum sativum) roots were investigated. Compared with the control treatment without Al, the accumulation of Al in tobacco cells caused instantaneously the repression of mitochondrial activities [monitored by the reduction of 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide and the uptake of Rhodamine 123] 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 Al-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 butylated hydroxyanisol can be a mechanism of Al tolerance. In the pea root, Al also triggered ROS production, respiration inhibition, and ATP depletion, which were all correlated with inhibition of root elongation. Taken together, we conclude that Al affects mitochondrial functions, which leads to ROS production, probably the key critical event in Al inhibition of cell growth.Al is a most abundant metal in the earth's crust and is solubilized as the free Al 3ϩ ion under acidic conditions. A wide range of toxic effects of Al ions has been demonstrated in plants and animals, although the mechanisms of Al toxicity have not been elucidated. In animals, Al is a potent neurotoxin, whereas in plants, Al is a major factor reducing crop production in acid soils (for review, see
Potential mechanisms of Al toxicity measured as Al-induced inhibition of growth in cultured tobacco cells (Nicotiana tabacum, nonchlorophyllic cell line SL) and pea (Pisum sativum) roots were investigated. Compared with the control treatment without Al, the accumulation of Al in tobacco cells caused instantaneously the repression of mitochondrial activities [monitored by the reduction of 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide and the uptake of Rhodamine 123] 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 Al-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 butylated hydroxyanisol can be a mechanism of Al tolerance. In the pea root, Al also triggered ROS production, respiration inhibition, and ATP depletion, which were all correlated with inhibition of root elongation. Taken together, we conclude that Al affects mitochondrial functions, which leads to ROS production, probably the key critical event in Al inhibition of cell growth.Al is a most abundant metal in the earth's crust and is solubilized as the free Al 3ϩ ion under acidic conditions. A wide range of toxic effects of Al ions has been demonstrated in plants and animals, although the mechanisms of Al toxicity have not been elucidated. In animals, Al is a potent neurotoxin, whereas in plants, Al is a major factor reducing crop production in acid soils (for review, see
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