Phytoremediation is optimized when plants grow vigorously while accumulating the contaminant of interest. Here we show that sulphur supply alleviates aerial chlorosis and growth retardation caused by cesium stress without reducing cesium accumulation in Arabidopsis thaliana. This alleviation was not due to recovery of cesium-induced potassium decrease in plant tissues. Sulphur supply also alleviated sodium stress but not potassium deficiency stress. Cesium-induced root growth inhibition has previously been demonstrated as being mediated through jasmonate biosynthesis and signalling but it was found that sulphur supply did not decrease the levels of jasmonate accumulation or jasmonate-responsive transcripts. Instead, induction of a glutathione synthetase gene GSH2 and reduction of a phytochelatin synthase gene PCS1 as well as increased accumulation of glutathione and cysteine were observed in response to cesium. Exogenous application of glutathione or concomitant treatments of its biosynthetic intermediates indeed alleviated cesium stress. Interestingly, concomitant treatments of glutathione biosynthetic intermediates together with a glutathione biosynthesis inhibitor did not cancel the alleviatory effects against cesium suggesting the existence of a glutathione-independent pathway. Taken together, our findings demonstrate that plants exposed to cesium increase glutathione accumulation to alleviate the deleterious effects of cesium and that exogenous application of sulphur-containing compounds promotes this innate process.

Cesium has no known beneficial effects on plants and while plants have the ability to absorb it through the root system, plant growth is retarded at high concentrations. Recently, we have shown that potassium influx through a potassium channel complex AKT1-KC1 is inhibited by cesium in Arabidopsis thaliana and the resultant reduction in potassium accumulation in the plant is the primary cause of retarded growth. By contrast, a major potassium transporter, HAK5 whose function is crucial under potassium deficiency, was found to be either not affected or complementary under cesium stress in the low affinity potassium range. Here we show the effects of insertional mutation on other members of KUP/HAK/KT gene family in response to cesium stress. Potassium and cesium concentrations in each mutant line demonstrated that disruption of a single KUP/HAK/KT gene was not sufficient to significantly reduce potassium/cesium accumulation, suggesting a complementary effect among these KUP (K + UPTAKE PERMEASE) transporters.

Phytoaccumulation is a technique to extract metals from soil utilising ability of plants. Cesium is a valuable metal while radioactive isotopes of cesium can be hazardous. In order to establish a more efficient phytoaccumulation system, small molecules which promote plants to accumulate cesium were investigated. Through chemical library screening, 14 chemicals were isolated as ‘cesium accumulators’ in Arabidopsis thaliana. Of those, methyl cysteinate, a derivative of cysteine, was found to function within the plant to accumulate externally supplemented cesium. Moreover, metabolite profiling demonstrated that cesium treatment increased cysteine levels in Arabidopsis. The cesium accumulation effect was not observed for other cysteine derivatives or amino acids on the cysteine metabolic pathway tested. Our results suggest that methyl cysteinate, potentially metabolised from cysteine, binds with cesium on the surface of the roots or inside plant cells and improve phytoaccumulation.

Cesium (Cs+) is known to compete with the macronutrient potassium (K+) inside and outside of plants and inhibit plant growth at high concentrations. However, the detailed molecular mechanisms of how Cs+ exerts its deleterious effects on K+ accumulation in plants are not fully elucidated. Here, we show that mutation in a member of the major K+ channel AKT1-KC1 complex renders Arabidopsis thaliana hypersensitive to Cs+. Higher severity of the phenotype and K+ loss was observed for these mutants in response to Cs+ than to K+ deficiency. Electrophysiological analysis demonstrated that Cs+, but not sodium, rubidium or ammonium, specifically inhibited K+ influx through the AKT1-KC1 complex. By contrast, Cs+ did not inhibit K+ efflux through the homomeric AKT1 channel that occurs in the absence of KC1, leading to a vast loss of K+. Our observation suggests that reduced K+ accumulation due to blockage/competition in AKT1 and other K+ transporters/channels by Cs+ plays a major role in plant growth retardation. This report describes the mechanical role of Cs+ in K+ accumulation, and in turn in plant performance, providing actual evidence at the plant level to what has long been believed; K+ channels are, therefore AKT1 is, "blocked" by Cs+.

Cesium (Cs) is found at low levels in nature but does not confer any known benefit to plants. Cs and K compete in cells due to the chemical similarity of Cs to potassium (K), and can induce K deficiency in cells. In previous studies, we identified chemicals that increase Cs tolerance in plants. Among them, a small chemical compound (C17H19F3N2O2), named CsToAcE1, was confirmed to enhance Cs tolerance while increasing Cs accumulation in plants. Treatment of plants with CsToAcE1 resulted in greater Cs and K accumulation and also alleviated Cs-induced growth retardation in Arabidopsis. In the present study, potential target proteins of CsToAcE1 were isolated from Arabidopsis to determine the mechanism by which CsToAcE1 alleviates Cs stress, while enhancing Cs accumulation. Our analysis identified one of the interacting target proteins of CsToAcE1 to be BETA-GLUCOSIDASE 23 (AtβGLU23). Interestingly, Arabidopsis atβglu23 mutants exhibited enhanced tolerance to Cs stress but did not respond to the application of CsToAcE1. Notably, application of CsToAcE1 resulted in a reduction of Cs-induced AtβGLU23 expression in wild-type plants, while this was not observed in a high affinity transporter mutant, athak5. Our data indicate that AtβGLU23 regulates plant response to Cs stress and that CsToAcE1 enhances Cs tolerance by repressing AtβGLU23. In addition, AtHAK5 also appears to be involved in this response.