Abstract
BackgroundFe toxicity occurs in lowland rice production due to excess ferrous iron (Fe2+) formation in reduced soils. To contribute to the breeding for tolerance to Fe toxicity in rice, we determined quantitative trait loci (QTL) by screening two different bi-parental mapping populations under iron pulse stresses (1,000 mg L−1 = 17.9 mM Fe2+ for 5 days) in hydroponic solution, followed by experiments with selected lines to determine whether QTLs were associated with iron exclusion (i.e. root based mechanisms), or iron inclusion (i.e. shoot-based mechanisms).ResultsIn an IR29/Pokkali F8 recombinant inbred population, 7 QTLs were detected for leaf bronzing score on chromosome 1, 2, 4, 7 and 12, respectively, individually explaining 9.2-18.7% of the phenotypic variation. Two tolerant recombinant inbred lines carrying putative QTLs were selected for further experiments. Based on Fe uptake into the shoot, the dominant tolerance mechanism of the tolerant line FL510 was determined to be exclusion with its root architecture being conducive to air transport and thus the ability to oxidize Fe2+ in rhizosphere. In line FL483, the iron tolerance was related mainly to shoot-based mechanisms (tolerant inclusion mechanism). In a Nipponbare/Kasalath/Nipponbare backcross inbred population, 3 QTLs were mapped on chromosomes 1, 3 and 8, respectively. These QTLs explained 11.6-18.6% of the total phenotypic variation. The effect of QTLs on chromosome 1 and 3 were confirmed by using chromosome segment substitution lines (SL), carrying Kasalath introgressions in the genetic background on Nipponbare. The Fe uptake in shoots of substitution lines suggests that the effect of the QTL on chromosome 1 was associated with shoot tolerance while the QTL on chromosome 3 was associated with iron exclusion.ConclusionTolerance of certain genotypes were classified into shoot- and root- based mechanisms. Comparing our findings with previously reported QTLs for iron toxicity tolerance, we identified co-localization for some QTLs in both pluse and chronic stresses, especially on chromosome 1.
Highlights
Fe toxicity occurs in lowland rice production due to excess ferrous iron (Fe2+) formation in reduced soils
In an IR29/Pokkali F8 recombinant inbred population, 7 quantitative trait loci (QTL) were detected for leaf bronzing score on chromosome 1, 2, 4, 7 and 12, respectively, individually explaining 9.2-18.7% of the phenotypic variation
The Fe uptake in shoots of substitution lines suggests that the effect of the QTL on chromosome 1 was associated with shoot tolerance while the QTL on chromosome 3 was associated with iron exclusion
Summary
Fe toxicity occurs in lowland rice production due to excess ferrous iron (Fe2+) formation in reduced soils. In anaerobic soils and at low redox potential (Eh), Fe is reduced to its soluble form Fe2+ and can be taken up excessively by plants. Several types of Fe toxic conditions occur, differing by landscape and soil type attributes, the Fe concentrations in the solutions, and the physiological stage at which the stress occurs. (i) Due to high content of Fe2+ in acid sulfate soils, toxicity symptoms on plants can be observed during the whole growth period. Leaf bronzing symptoms appear mainly during the late vegetative growth stage while genotypes are transplanted in the dry season with high vapor pressure deficits. Yield losses can range from 30-70%, but when severe toxicity occurs at the seedling stage, total crop failure can occur. Water and nutrient management strategies have been suggested to counteract negative effects of excess Fe in solution, the most promising approach is to use tolerant genotypes
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