Elimination of FRDL1, a xylem-located citrate transporter, confers tolerance to excess unchelated ferrous iron through an exclusion mechanism in rice (Oryza sativa L.).

Abstract

Iron (Fe) toxicity is a common agricultural problem that limits rice yield in various regions of Southeast Asia and Africa. Previous studies have proposed physiological mechanisms for tolerance, but the specific genes associated with these mechanisms are largely unknown. In this study, I hypothesized that organic acids play a crucial role in Fe toxicity tolerance in rice and evaluated retrotransposon-insertion mutant lines of citrate transporters under Fe toxicity stress in hydroponics. Fe toxicity-induced leaf bronzing and Fe concentrations were measured. A knock-down line of the xylem-localized citrate transporter, FRDL1, had a significantly lower degree of leaf bronzing symptoms under Fe toxicity when unchelated ferrous iron (Fe²⁺, as FeSO₄), but not chelated ferric iron (as Fe(III)-EDTA), was used as Fe source. The knock-down line of FRDL1 had lower Fe concentrations in leaf blades, while concentrations in stems and roots were unaffected under excess ferrous iron conditions. Knock-down of FRDL1 also reduced foliar Fe concentrations and leaf bronzing symptoms in Ciherang, an indica variety that is highly sensitive to Fe toxicity stress. This study highlights that low xylem citrate concentrations restrict translocation of excess Fe to leaves, suggesting a novel physiological aspect for improved Fe toxicity tolerance in rice. This study also suggests that selection of the Fe source is crucial in Fe toxicity experiments.