Genetic variation in Fe toxicity tolerance is associated with the regulation of translocation and chelation of iron along with antioxidant defence in shoots of rice

Ahmad Humayan Kabir; Most Champa Begum; Ariful Haque; Ruhul Amin; A M Swaraz; Syed Ali Haider; Nishit Kumar Paul; Mohammad Monzur Hossain

doi:10.1071/FP16068

Genetic variation in Fe toxicity tolerance is associated with the regulation of translocation and chelation of iron along with antioxidant defence in shoots of rice

Funct Plant Biol. 2016 Nov;43(11):1070-1081. doi: 10.1071/FP16068.

Authors

Ahmad Humayan Kabir¹, Most Champa Begum¹, Ariful Haque², Ruhul Amin³, A M Swaraz⁴, Syed Ali Haider¹, Nishit Kumar Paul¹, Mohammad Monzur Hossain¹

Affiliations

¹ Plant and Crop Physiology Laboratory, Department of Botany, University of Rajshahi, Rajshahi 6205, Bangladesh.
² Institute of Biological Sciences, University of Rajshahi, Rajshahi 6205, Bangladesh.
³ Bangladesh Council of Scientific and Industrial Research (BCSIR) Laboratories, Rajshahi 6206, Bangladesh.
⁴ Department of Genetic Engineering and Biotechnology, Jessore University of Science and Technology, Jessore 7408, Bangladesh.

PMID: 32480527
DOI: 10.1071/FP16068

Abstract

Excess iron (Fe) is phytotoxic and causes reduced growth and productivity in rice. In this study we elucidated the mechanisms conferring differential tolerance to Fe-toxicity in rice seedlings. Excess Fe caused retardation in roots of both Pokkali and BRRI 51, but it caused no significant changes on growth parameters, Fe accumulation and OsIRT1 expression in shoots of Pokkali only compared with control plants. These results suggest that the Pokkali genotype does have mechanisms in shoots to withstand Fe toxicity. Pokkali maintained membrane stability and total soluble protein in shoots due to Fe toxicity, further confirming its ability to tolerate excess Fe. Furthermore, a significant decrease of Fe-chelate reductase activity and OsFRO1 expression in shoots of Pokkali suggests that limiting Fe accumulation is possibly regulated by Fe-reductase activity. Our extensive expression analysis on the expression pattern of three chelators (OsDMAS1, OsYSL15, OsYSL2 and OsFRDL1) showed no significant changes in expression in shoots of Pokkali due to Fe toxicity, whereas these genes were significantly upregulated under Fe-toxicity in sensitive BRRI 51. These results imply that regulation of Fe chelation in shoots of Pokkali contributes to its tolerance to Fe toxicity. Finally, increased catalase (CAT), peroxidase (POD), glutathione reductase (GR) and superoxide dismutase (SOD), along with elevated ascorbic acid, glutathione, cysteine, methionine and proline in shoots of Pokkali caused by Fe toxicity suggests that strong antioxidant defence protects rice plants from oxidative injury under Fe toxicity. Taking these results together, we propose that genetic variation in Fe-toxicity tolerance in rice is shoot based, and is mainly associated with the regulation of translocation and chelation of Fe together with elevated antioxidant metabolites in shoots.