Quantitative trait loci controlling aluminium tolerance in two accessions of <i>Arabidopsis thaliana</i> (Landsberg <i>erecta</i> and Cape Verde Islands)

Kobayashi, Yuriko; Furuta, Yachiyo; Ohno, Takashi; Hara, Tetsuo; Koyama, Hiroyuki

doi:10.1111/j.1365-3040.2005.01388.x

Cited by 33 publications

(35 citation statements)

References 57 publications

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“…In both Landsberg erecta (Ler) 3 Columbia (Col) and Ler 3 Cape Verde Islands populations, the major Al tolerance QTLs were consistent with the position of an Arabidopsis homolog of the TaALMT1 (Kobayashi and Koyama, 2002;Hoekenga et al, 2003;Sasaki et al, 2004;Kobayashi et al, 2005). Analysis of a knockout mutant for the AtALMT1 locus confirmed the importance and uniqueness for this member of the AtALMT gene family (Hoekenga et al, 2006).…”

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confidence: 69%

“…Al-activated OA release, specifically malate, was first associated with Al tolerance in Arabidopsis (Arabidopsis thaliana) via a series of quantitative trait locus (QTL) studies (Hoekenga et al, 2003;Kobayashi et al, 2005). In both Landsberg erecta (Ler) 3 Columbia (Col) and Ler 3 Cape Verde Islands populations, the major Al tolerance QTLs were consistent with the position of an Arabidopsis homolog of the TaALMT1 (Kobayashi and Koyama, 2002;Hoekenga et al, 2003;Sasaki et al, 2004;Kobayashi et al, 2005).…”

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confidence: 95%

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Characterization of AtALMT1 Expression in Aluminum-Inducible Malate Release and Its Role for Rhizotoxic Stress Tolerance in Arabidopsis

et al. 2007

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Malate transporters play a critical role in aluminum (Al) tolerance responses for some plant species, such as Arabidopsis (Arabidopsis thaliana). Here, we further characterize AtALMT1, an Arabidopsis aluminum-activated malate transporter, to clarify its specific role in malate release and Al stress responses. Malate excretion from the roots of accession Columbia was sharply induced by Al, which is concomitant with the induction of AtALMT1 gene expression. The malate release was specific for Al among rhizotoxic stressors, namely cadmium, copper, erbium, lanthanum, sodium, and low pH, which accounts for the specific sensitivity of a null mutant to Al stress. Al-specific malate excretion can be explained by a combined regulation of AtALMT1 expression and activation of AtALMT1 protein, which is specific for Al. Although low pH treatment slightly induced gene expression, other treatments did not. In addition, malate excretion in Al-activated seedlings was rapidly stopped by removing Al from the solution. Other rhizotoxic stressors were not effective in maintaining malate release. Protein kinase and phosphatase inhibitor studies indicated that reversible phosphorylation was important for the transcriptional and posttranslational regulation of AtALMT1. AtALMT1 promoter-β-glucuronidase fusion lines revealed that AtALMT1 has restricted expression within the root, such that unnecessary carbon loss is likely minimized. Lastly, a natural nonsense mutation allele of AtALMT1 was identified from the Al-hypersensitive natural accession Warschau-1.

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confidence: 69%

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Characterization of AtALMT1 Expression in Aluminum-Inducible Malate Release and Its Role for Rhizotoxic Stress Tolerance in Arabidopsis

et al. 2007

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“…The properties of these soils are well characterized and used in physiological experiments for Al and proton toxicities . The soil was fertilized with both macronutrients and micronutrients as described previously (Kobayashi et al, 2005). Kawatabi soil was neutralized by adding CaCO 3 (60, 250, and 400 mg per 100 g of dry soil).…”

Section: Methodsmentioning

confidence: 99%

“…To evaluate the Al sensitivity of these KO mutants, we employed a relatively high pH to minimize the effect of H 1 toxicity. pH 5.0 was previously used in quantitative trait locus analyses of Al tolerance (Kobayashi et al, 2005;Ikka et al, 2008), while pH 5.5 was also employed to minimize H 1 rhizotoxicity in this study. Under both conditions, ALS3-KO showed a hypersensitive phenotype to Al in comparison with the wild type, while it was significantly more resistant than STOP1-KO and AtALMT1-KO (Fig.…”

Section: Down-regulation Of Als3 In the Stop1 Mutantmentioning

confidence: 99%

STOP1 Regulates Multiple Genes That Protect Arabidopsis from Proton and Aluminum Toxicities

et al. 2009

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The Arabidopsis (Arabidopsis thaliana) mutant stop1 (for sensitive to proton rhizotoxicity1) carries a missense mutation at an essential domain of the histidine-2-cysteine-2 zinc finger protein STOP1. Transcriptome analyses revealed that various genes were down-regulated in the mutant, indicating that STOP1 is involved in signal transduction pathways regulating aluminum (Al)- and H+-responsive gene expression. The Al hypersensitivity of the mutant could be caused by down-regulation of AtALMT1 (for Arabidopsis ALUMINUM-ACTIVATED MALATE TRANSPORTER1) and ALS3 (ALUMINUM-SENSITIVE3). This hypothesis was supported by comparison of Al tolerance among T-DNA insertion lines and a transgenic stop mutant carrying cauliflower mosaic virus 35S∷AtALMT1. All T-DNA insertion lines of STOP1, AtALMT1, and ALS3 were sensitive to Al, but introduction of cauliflower mosaic virus 35S∷AtALMT1 did not completely restore the Al tolerance of the stop1 mutant. Down-regulation of various genes involved in ion homeostasis and pH-regulating metabolism in the mutant was also identified by microarray analyses. CBL-INTERACTING PROTEIN KINASE23, regulating a major K+ transporter, and a sulfate transporter, SULT3;5, were down-regulated in the mutant. In addition, integral profiling of the metabolites and transcripts revealed that pH-regulating metabolic pathways, such as the γ-aminobutyric acid shunt and biochemical pH stat pathways, are down-regulated in the mutant. These changes could explain the H+ hypersensitivity of the mutant and would make the mutant more susceptible in acid soil stress than other Al-hypersensitive T-DNA insertion lines. Finally, we showed that STOP1 is localized to the nucleus, suggesting that the protein regulates the expression of multiple genes that protect Arabidopsis from Al and H+ toxicities, possibly as a transcription factor.

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“…Growth experiments in hydroponics were carried out with the hydroponic culture system used for an Al-tolerant quantitative trait loci study (39). Briefly, seedlings were grown in test solutions containing various toxicants for the root growth within the control solution, namely modified MGRL medium (40) (1/50 strength but with Pi eliminated and Ca concentration adjusted to 200 M).…”

Section: Methodsmentioning

confidence: 99%

Zinc finger protein STOP1 is critical for proton tolerance in Arabidopsis and coregulates a key gene in aluminum tolerance

Iuchi

Koyama

Iuchi

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

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Acid soil syndrome causes severe yield losses in various crop plants because of the rhizotoxicities of ions, such as aluminum (Al 3؉ ). Although protons (H ؉ ) could be also major rhizotoxicants in some soil types, molecular mechanisms of their tolerance have not been identified yet. One mutant that was hypersensitive to H ؉ rhizotoxicity was isolated from ethyl methanesulfonate mutagenized seeds, and a single recessive mutation was found on chromosome 1. Positional cloning followed by genomic sequence analysis revealed that a missense mutation in the zinc finger domain in a predicted Cys2His2-type zinc finger protein, namely sensitive to proton rhizotoxicity (STOP)1, is the cause of hypersensitivity to H ؉ rhizotoxicity. The STOP1 protein belongs to a functionally unidentified subfamily of zinc finger proteins, which consists of two members in Arabidopsis based on a Blast search. The stop1 mutation resulted in no effects on cadmium, copper, lanthanum, manganese and sodium chloride sensitivitities, whereas it caused hypersensitivity to Al 3؉ rhizotoxicity. This stop1 mutant lacked the induction of the AtALMT1 gene encoding a malate transporter, which is concomitant with Al-induced malate exudation. There was no induction of AtALMT1 by Al 3؉ treatment in the stop1 mutant. These results indicate that STOP1 plays a critical role in Arabidopsis tolerance to major stress factors in acid soils. aluminum toxicity ͉ Arabidopsis thaliana ͉ Cys2His2-type zinc finger protein ͉ proton-rhizotoxicity ͉ sensitive to proton rhizotoxicity

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Quantitative trait loci controlling aluminium tolerance in two accessions of Arabidopsis thaliana (Landsberg erecta and Cape Verde Islands)

Abstract: ABSTRACT

Cited by 33 publications

References 57 publications

Characterization of AtALMT1 Expression in Aluminum-Inducible Malate Release and Its Role for Rhizotoxic Stress Tolerance in Arabidopsis

Characterization of AtALMT1 Expression in Aluminum-Inducible Malate Release and Its Role for Rhizotoxic Stress Tolerance in Arabidopsis

STOP1 Regulates Multiple Genes That Protect Arabidopsis from Proton and Aluminum Toxicities

Zinc finger protein STOP1 is critical for proton tolerance in Arabidopsis and coregulates a key gene in aluminum tolerance

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