Abstract

Iron toxicity is one of the most widely spread mineral disorders in anaerobic soils, but the tolerance mechanisms in plants are poorly understood. Here we characterize the involvement of a rice potassium ion channel gene, OsAKT1, in Fe toxic conditions. Two knock-down lines of OsAKT1 together with azygos lines were investigated. Mutant lines did not differ from azygos lines regarding plant growth, gas exchange rate or chlorophyll fluorescence in control conditions. However, loss-of-function of OsAKT1 increased the sensitivity to excess Fe regarding leaf bronzing symptoms, reactive oxygen species generation, leaf spectral reflectance indices, and chlorophyll fluorescence. Fe toxicity leads to largely reduced uptake of other nutrients into shoots, which illustrates the complexity of Fe stress related to multiple mineral disorders. Less potassium uptake in the mutants compared to azygos lines co-occurred with higher amounts of Fe accumulated in the shoot tissues but not in the roots. These results were consistent with a higher level of Fe loaded into the xylem sap of mutants compared to azygos lines in the early phase of Fe toxicity. In conclusion, OsAKT1 is crucial for the tolerance of rice against Fe toxicity as K homeostasis affects Fe translocation from root to shoot.

Highlights

  • Iron (Fe) is a crucial mineral element for all living organisms due to its property as an electron receptor/donor (Kobayashi et al, 2013)

  • The results indicate the crucial roles of OsAKT1 in the tolerance to Fe toxicity in rice

  • We investigated a potassium ion channel gene OsAKT1, which was nominated as a candidate gene underlying an Fe uptake quantitative trait loci (QTL) in our previous study (Matthus et al, 2015)

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Summary

Introduction

Iron (Fe) is a crucial mineral element for all living organisms due to its property as an electron receptor/donor (Kobayashi et al, 2013). Despite its various roles in photosynthesis, respiration and other physiological processes in plants, Fe is toxic when presenting in excess (Becker and Asch, 2005). In lowland rice fields that contribute 95% of the world rice production, Fe prevalently occurs in the reduced and soluble ferrous form (Fe2+) due to the low soil redox potential arising from anaerobic conditions, which are formed when soil microorganisms and plant roots deplete oxygen by respiration. Excessive Fe2+ are transported via the xylem flow to the shoot leading to Fe toxicity, which is one of the most widely observed nutrient disorders in lowland rice production (Becker and Asch, 2005; Frei et al, 2016). Fe2+ is oxidized to Fe3+, which can be reduced back to Fe2+ by reducing agents such as ascorbate

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