Pharmacological and gene regulation properties point to the SlHAK5 K+ transporter as a system for high-affinity Cs+ uptake in tomato plants.

Potassium (K+ ) and cesium (Cs+ ) are chemically similar but while K+ is an essential nutrient, Cs+ can be toxic for living organisms, plants included. Two different situations could lead to problems derived from the presence of Cs+ in agricultural systems: (1) presence of Cs+ at high concentrations that could produce toxic effects on plants, (2) presence of micromolar concentrations of radiocesium, which can be accumulated in the plant and affect animal and human health through the food chain. While K+ uptake has been well described in tomato plants, information on molecular mechanisms involved in Cs+ accumulation in this species is absent. Here, we show that in tomato plants, high concentrations of Cs+ produce deficiency of K+ but do not induce high-affinity K+ uptake or the gene encoding the high-affinity K+ transporter SlHAK5. At these concentrations, Cs+ uptake takes place through a Ca2+ -sensitive pathway, probably a non-selective cation channel. At micromolar concentrations, Cs+ is accumulated by a high-affinity uptake system upregulated in K+ -starved plants. This high-affinity Cs+ uptake shares features with high-affinity K+ uptake. It is sensitive to NH4+ and insensitive to Ba2+ and Ca2+ and its presence parallels the pattern of SlHAK5 expression. Moreover, blockers of reactive oxygen species and ethylene action repress SlHAK5 and negatively regulate both high-affinity K+ and Cs+ uptake. Thus, we propose that SlHAK5 contributes to Cs+ uptake from micromolar concentrations in tomato plants and can constitute a pathway for radiocesium transfer from contaminated areas to the food chain.