Plant Science

Biography

Biography: Ryoung Shin

Abstract

Cesium (Cs⁺) exists in nature at relatively low levels but occasionally accidental anthropogenic activities spread high levels of Cs⁺ (most commonly radioactive) which contaminate the environment and enter the food chain. Cs⁺ disrupts plant growth at high concentrations through pleiotropic effects and the part of the Cs⁺ toxicity in plants is known to derive from competition and interference with potassium (K⁺) due to the similarity in physicochemical properties between K⁺ and Cs⁺. K⁺ is an essential nutrient, a lack of which causes serious growth retardation and physiological defects. In order to find the means to sustain plant growth in Cs⁺-contaminated areas for phytoremediation purpose, the molecular mechanisms of how Cs⁺ exerts its deleterious effects on K⁺ accumulation in plants need to be elucidated. In Arabidopsis thaliana, K⁺ uptake through the roots is considered to be mediated mainly by two players: Arabidopsis K⁺ Transporter 1 (AKT1) and High Affinity K⁺ Transporter 5 (HAK5). Expression of HAK5 is swiftly induced in response to K⁺ deficiency while AKT1 is more responsible for low-affinity K⁺ uptake. AKT1 forms a tetrameric complex with K⁺ Rectifying Channel 1 (KC1) to exert proper function. Here, we show that mutation on a member of the major K⁺ channel AKT1-KC1 complex renders Arabidopsis thaliana hypersensitive to Cs⁺. Electrophysiological analysis demonstrated that Cs⁺, but not sodium, rubidium or ammonium, specifically inhibited K⁺ influx through the AKT1-KC1 complex. In addition, a lack of KC1 further led to an inability of Arabidopsis to accumulate K⁺ in the plant body due to uncontrollable K⁺ leakage through the homomeric AKT1 channel. These data indicate that Cs⁺ is a specific inhibitor of the AKT1 complex-mediated K⁺ influx and KC1 is essential to avoid K⁺ leakage.