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

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.

Arbuscular Mycorrhizal Symbiosis Mitigates Iron (Fe)-Deficiency Retardation in Alfalfa (Medicago sativa L.) Through the Enhancement of Fe Accumulation and Sulfur-Assisted Antioxidant Defense

“…GR is an important antioxidant that acts against H 2 O 2 and O 2 − [45]. Further, this enzyme is essential for GSH, an S-metabolite that protects the cell from oxidative damage [46]. This phenomenon was also consistently supported the increased GSH and cysteine accumulation in alfalfa roots, as evident by our HPLC analysis due to AMF treatment under Fe deficiency.…”

Iron toxicity-induced physiological and metabolite profile variations among tolerant and sensitive rice varieties

“…IR64 and Inpara 5 as sensitive varieties to Fe toxicity stress, 35,36 Inpara 2 is categorized as a moderate tolerant variety to Fe toxicity stress, 36 while Pokkali is categorized as a tolerant variety. 17,[35][36][37] Fe toxicity stress disturbs metabolisms in plant, which is manifested as the formation of leaf bronzing that causes a reduction in plant growth and yield. 6,27,36,38 The bronzing symptom begins at the tips of the oldest leaves and spreads throughout the leaves.…”

Biochemical and molecular mechanisms associated with Zn deficiency tolerance and signaling in rice (Oryza sativa L.)

“…Recently, a five-fold increase of proline accumulation was reported in Zn-efficient RIL47 cultivar under Zn deficiency (Höller, Hajirezaei, et al 2014). Studies revealed that abiotic stress tolerance is associated with ROS scavenging via increased antioxidant defense (Alscher et al 2002;Hacisalihoglu et al 2003;Kabir et al 2016).…”