Polymorphism and physiology of arsenate tolerance in Holcus lanatus L. from an uncontaminated site

Meharg, Andrew A.; Macnair, Mark R.

doi:10.1007/bf00012015

Cited by 36 publications

(27 citation statements)

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“…Even when the As : P ratio of the soil is as high as 200, the As : P ratio in the plant does not rise above 0.5 (Meharg et al, 1994). This was also found in our experiment where the As : P ratio within the plant never exceeded 0.27, even in the low-phosphate treatment in which the As : P ratio in the nutrient solution was 10 (data not shown).Root length growth has been used by various authors to determine the toxicity of arsenate (Rocovich & West, 1975 ;Porter & Peterson, 1977 ;Pollard, 1980 ;Paliouris & Hutchinson, 1991 ; De Koe et al, 1992 ;Macnair et al, 1992 ;Meharg & Macnair, 1992a ;Meharg et al, 1993). However, these tests were always performed over short time periods.…”

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confidence: 85%

“…Toxicity of As in plants has been studied most extensively in grasses (Rocovich & West, 1975 ;Porter & Peterson, 1977 ;Pollard, 1980 ; De Koe et al., 1992 ;Macnair et al, 1992 ;Meharg & Macnair, 1992a ;Meharg et al, 1993), although some work has been published on dicotyledonous species (Paliouris & Hutchinson, 1991). However, these were all shortterm studies, and the toxicity of As in chronically exposed plants remains unclear.…”

Section: mentioning

confidence: 99%

“…Root length growth has been used by various authors to determine the toxicity of arsenate (Rocovich & West, 1975 ;Porter & Peterson, 1977 ;Pollard, 1980 ;Paliouris & Hutchinson, 1991 ; De Koe et al, 1992 ;Macnair et al, 1992 ;Meharg & Macnair, 1992a ;Meharg et al, 1993). However, these tests were always performed over short time periods.…”

Section: mentioning

confidence: 99%

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Toxicity of arsenate in Silene vulgaris, accumulation and degradation of arsenate‐induced phytochelatins

et al. 1999

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The results presented in this paper describe the short-and long-term toxicity of arsenate in Silene vulgaris. Shortterm toxicity, measured as inhibition of root elongation, depended on phosphate nutrition, arsenate being much less toxic at high phosphate supply. At low phosphate levels more arsenic was taken up by the plants. Under chronic exposure, toxicity (measured as inhibition of biomass production) did not increase with time. In addition, the accumulation of phytochelatins (PCs) as a function of toxicity and duration of exposure was studied. Shortterm PC accumulation (over a 3 d period) was positively correlated with exposure. Isolation of peptide complexes from prolongedly exposed plants showed that PC # , PC $ and PC % were present, although the latter not until at least 3 d exposure. Arsenic co-eluted mainly with PC # and PC $ . Fractions containing PC % were devoid of As, probably due to dissociation of the complexes during extraction or elution. The breakdown of PCs after arresting As exposure was very slow. This could explain the continuous accumulation of PCs throughout longer periods of As exposure.Key words : Silene vulgaris, arsenic toxicity, arsenic detoxification, phytochelatins. Arsenic is taken up mainly by plant roots as arsenate (AsO % $−) (Macnair & Cumbes, 1987) through the phosphate-uptake system (Asher & Reay, 1979). Once the arsenate, As(V), is taken up it is reduced to arsenite, As(III), by glutathione (GSH) (Thompson, 1993). Only in phosphate-deficient conditions is arsenate subsequently methylated in plants (Nissen & Benson, 1982). Between the successive methylation steps, GSH serves to reduce the intermediate products (Scott et al., 1993 ;Thompson, 1993). Arsoniumphospholipids in freshwater plants (Nissen & Benson, 1982) and arsenic sugars in marine brown algae (Edmonds & Francesconi, 1981) have also been identified.Mostly there is little transport of As to the aboveground parts of the plants. Dicotyledonous plants appear to transport more As to the shoots than monocotyledonous plants (Otte, 1991). The form in *Author for correspondence (fax j31 20 444 7123 ; e-mail elsesnel!bio.vu.nl). which the As is transported is unknown. There is some indication that dimethylarsenic acid is transported to the shoots (Marin et al., 1993).Increased As levels may cause toxic symptoms in plants, such as a decrease in plant growth and fruit yield (Carbonell-Barrachina et al., 1995), root discoloration and root plasmolysis, wilting and necrosis of leaf tips and leaf margins (Machlis, 1941), and a decrease in photosynthetic capacity (Marin et al., 1993).Some authors have reported the accumulation of heavy metal-binding, thiol-rich phytochelatins (PCs) on exposure to As (Grill et al., 1986a(Grill et al., ,b, 1987Maitani et al., 1996). Phytochelatins have the structure (γ-glu-cys) n -gly, where n l 2-11 (Grill et al., 1985), and are produced in plants on exposure to a variety of heavy metals and metalloids (Gekeler et al., 1989). Phytochelatins are synthesized from GSH (Hayashi et ...

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confidence: 85%

Section: mentioning

confidence: 99%

Section: mentioning

confidence: 99%

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Toxicity of arsenate in Silene vulgaris, accumulation and degradation of arsenate‐induced phytochelatins

et al. 1999

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“…Holcus lanatus is frequently found growing on arsenate-contaminated mine spoil soils, and it achieves arsenate resistance through suppression of the high-affinity P-arsenate uptake system (HAUS) (Meharg & Macnair, 1990, 1992cMeharg et al, 1994b). Arsenate-resistant plants therefore have reduced P uptake and can be identified by a simple rooting test (Meharg & Macnair, 1992b). …”

Section: mentioning

confidence: 99%

Reproductive biomass in Holcus lanatus clones that differ in their phosphate uptake kinetics and mycorrhizal colonization

2000

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In normal populations of the common grass Holcus lanatus there is a polymorphism for arsenate resistance, manifested as suppressed phosphate uptake (SPU), and controlled by a major gene with dominant expression. A natural population of SPU plants had greater arbuscular-mycorrhizal colonization than wild type, nonSPU plants. It was hypothesized that, in order to survive alongside plants with a normal rate of phosphate (P) uptake, SPU plants would be more dependent on mycorrhizal associations. We performed an experiment using plants with SPU phenotypes from both arsenate mine spoils and uncontaminated soils, as well as plants with a nonSPU phenotype. They were grown with and without a mycorrhizal inoculum and added N, which altered plant P requirements. We showed that grasses with SPU phenotypes accumulated more shoot P than nonSPU plants, the opposite of the expected result. SPU plants also produced considerably more flower panicles, and had greater shoot and root biomass. The persistence of SPU phenotypes in normal populations is not necessarily related to mycorrhizal colonization as there were no differences in percentage AM colonization between the phenotypes. Being mycorrhizal reduced flower biomass production, as mycorrhizal SPU plants had lower shoot P concentrations and produced fewer flower panicles than non-mycorrhizal, nonSPU plants. We now hypothesize that the SPU phenotype is brought about by a genotype that results in increased accumulation of P in shoots, and that suppression of the rate of uptake is a consequence of this high shoot P concentration, operating by means of a homeostatic feedback mechanism. We also postulate that increased flower production is linked to a high shoot P concentration. SPU plants thus allocate more resources into seed production, leading to a higher frequency of SPU genes. Increased reproductive allocation reduces vegetative allocation and may affect competitive ability and hence survival, explaining the maintenance of the polymorphism. As mycorrhizal SPU plants behave more like nonSPU plants, AM colonization itself could play a major part in the maintenance of the SPU polymorphism.

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“…Populations from normal soils in Devon also have high frequencies, around 50%. In order to test the hypothesis that these high frequen-cies are simply the result of gene flow from contaminated sites on the granitic extrusion, Meharg et al (1993) (Meharg & Macnair, 19926). However, they also take up less phosphate, and it is difficult to believe that variation in phosphate nutrition can be a neutral character.…”

Section: The Occurrence Zvithin Normal Populationsmentioning

confidence: 99%

The genetics of metal tolerance in vascular plants

1993

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SUMMARY In many parts of the world soils are detrimental to plant growth owing to elevated levels of metal ions, caused either by natural processes or by the result of man's activities. Many plants have evolved ecotypes or varieties that are able to grow more‐or‐less normally on these soils. This paper reviews our knowledge of the genetics of this phenomenon. The nature of tolerance and the problems of its measurement are discussed. Tolerance is frequently measured by an index produced by comparing growth in a contaminated environment with growth in a control environment. It is argued that this measurement is inappropriate for many genetical studies, and that it is frequently more useful to use growth at a single critical level of metal as a measure of tolerance. Polygenic inheritance provides a null hypothesis that has to be tested in a genetical analysis. Examples of major genes for tolerance to aluminium, arsenic, boron, cadmium, copper and manganese are discussed. Even where major genes have been demonstrated, it is probable that other minor genes, ‘modifiers’, are present as well. Because of the nature of tolerance as a character, dominance and epistasis are likely to vary with the level of metal at which an analysis is performed. Tolerance is generally found to be dominant at some levels of the metal. Studies which have mapped tolerance genes, particularly to aluminium and salt, are discussed. The specificity of tolerance is a matter of some confusion. Some studies indicate that tolerances evolve independently to different metals, but others have suggested that tolerance to one metal may often confer a degree of tolerance to some other metals. Very little is known about the molecular genetics of tolerance, and the mechanisms of tolerance to most metals. The possible role of phytochelatins and metallothionein‐like proteins in metal tolerance is discussed. The distribution of tolerance in natural populations suggests that tolerance is a disadvantage in uncontaminated environments, but how this ‘cost’ arises is not known. There is some evidence that the disadvantage to tolerance may be associated more with the modifiers of tolerance than with the primary tolerance gene. The study of the genetics of tolerance is of importance in planning breeding programmes to produce tolerant crops for use in areas where metal contamination is a limiting factor in productivity. It can also assist in understanding the mechanisms of tolerance, as exemplified by the study of the mechanism of arsenic tolerance in Holcus lanatus. Important areas for further research are discussed.

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Polymorphism and physiology of arsenate tolerance in Holcus lanatus L. from an uncontaminated site

Cited by 36 publications

References 22 publications

Toxicity of arsenate in Silene vulgaris, accumulation and degradation of arsenate‐induced phytochelatins

Toxicity of arsenate in Silene vulgaris, accumulation and degradation of arsenate‐induced phytochelatins

Reproductive biomass in Holcus lanatus clones that differ in their phosphate uptake kinetics and mycorrhizal colonization

The genetics of metal tolerance in vascular plants

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