Arsenite provides a selective signal that coordinates arsenate uptake and detoxification through the regulation of PHR1 stability in Arabidopsis.

In nature, plants acquire nutrients from soils to sustain growth, and at the same time, they need to avoid the uptake of toxic compounds and/or possess tolerance systems to cope with them. This is particularly challenging when the toxic compound and the nutrient are chemically similar, as in the case of phosphate and arsenate. In this study, we demonstrated that regulatory elements of the phosphate starvation response (PSR) coordinate the arsenate detoxification machinery in the cell. We showed that arsenate repression of the phosphate transporter PHT1;1 is associated with the degradation of the PSR master regulator PHR1. Once arsenic is sequestered into the vacuole, PHR1 stability is restored and PHT1;1 expression is recovered. Furthermore, we identified an arsenite responsive SKP1-like protein and a PHR1 interactor F-box (PHIF1) as constituents of the SCF complex responsible for PHR1 degradation.We found that arsenite, the form to which arsenate is reduced for compartmentalization in vacuoles, represses PHT1;1 expression, providing a highly selective signal versus phosphate to control PHT1;1 expression in response to arsenate. Collectively, our results provide molecular insights into a sensing mechanism that regulates arsenate/phosphate uptake depending on the plant's detoxification capacity.

Cytokinin Determines Thiol-Mediated Arsenic Tolerance and Accumulation.

The presence of arsenic in soil and water is a constant threat to plant growth in many regions of the world. Phytohormones act in the integration of growth control and stress response, but their role in plant responses to arsenic remains to be elucidated. Here, we show that arsenate [As(V)], the most prevalent arsenic chemical species in nature, causes severe depletion of endogenous cytokinins (CKs) in the model plant Arabidopsis (Arabidopsis thaliana). We found that CK signaling mutants and transgenic plants with reduced endogenous CK levels showed an As(V)-tolerant phenotype. Our data indicate that in CK-depleted plants exposed to As(V), transcript levels of As(V)/phosphate-transporters were similar or even higher than in wild-type plants. In contrast, CK depletion provoked the coordinated activation of As(V) tolerance mechanisms, leading to the accumulation of thiol compounds such as phytochelatins and glutathione, which are essential for arsenic sequestration. Transgenic CK-deficient Arabidopsis and tobacco lines show a marked increase in arsenic accumulation. Our findings indicate that CK is an important regulatory factor in plant adaptation to arsenic stress.

Natural variation in arsenate tolerance identifies an arsenate reductase in Arabidopsis thaliana.

The enormous amount of environmental arsenic was a major factor in determining the biochemistry of incipient life forms early in the Earth's history. The most abundant chemical form in the reducing atmosphere was arsenite, which forced organisms to evolve strategies to manage this chemical species. Following the great oxygenation event, arsenite oxidized to arsenate and the action of arsenate reductases became a central survival requirement. The identity of a biologically relevant arsenate reductase in plants nonetheless continues to be debated. Here we identify a quantitative trait locus that encodes a novel arsenate reductase critical for arsenic tolerance in plants. Functional analyses indicate that several non-additive polymorphisms affect protein structure and account for the natural variation in arsenate reductase activity in Arabidopsis thaliana accessions. This study shows that arsenate reductases are an essential component for natural plant variation in As(V) tolerance.