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pubmed:abstractText |
The exceptional toxicity of arsenate [As(V)] is derived from its close chemical similarity to phosphate (Pi), which allows the metalloid to be easily incorporated into plant cells through the high-affinity Pi transport system. In this study, we identified an As(V)-tolerant mutant of Arabidopsis thaliana named pht1;1-3, which harbors a semidominant allele coding for the high-affinity Pi transporter PHT1;1. pht1;1-3 displays a slow rate of As(V) uptake that ultimately enables the mutant to accumulate double the arsenic found in wild-type plants. Overexpression of the mutant protein in wild-type plants provokes phenotypic effects similar to pht1;1-3 with regard to As(V) uptake and accumulation. In addition, gene expression analysis of wild-type and mutant plants revealed that, in Arabidopsis, As(V) represses the activation of genes specifically involved in Pi uptake, while inducing others transcriptionally regulated by As(V), suggesting that converse signaling pathways are involved in plant responses to As(V) and low Pi availability. Furthermore, the repression effect of As(V) on Pi starvation responses may reflect a regulatory mechanism to protect plants from the extreme toxicity of arsenic.
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