Nk Paul

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

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.

Regulation of Phytosiderophore Release and Antioxidant Defense in Roots Driven by Shoot-Based Auxin Signaling Confers Tolerance to Excess Iron in Wheat

Iron (Fe) is essential but harmful for plants at toxic level. However, how wheat plants tolerate excess Fe remains vague. This study aims at elucidating the mechanisms underlying tolerance to excess Fe in wheat. Higher Fe concentration caused morpho-physiological retardation in BR 26 (sensitive) but not in BR 27 (tolerant). Phytosiderophore and 2-deoxymugineic acid showed no changes in BR 27 but significantly increased in BR 26 due to excess Fe. Further, expression of TaSAMS. TaDMAS1, and TaYSL15 significantly downregulated in BR 27 roots, while these were upregulated in BR 26 under excess Fe. It confirms that inhibition of phytosiderophore directs less Fe accumulation in BR 27. However, phytochelatin and expression of TaPCS1 and TaMT1 showed no significant induction in response to excess Fe. Furthermore, excess Fe showed increased catalase, peroxidase, and glutathione reductase activities along with glutathione, cysteine, and proline accumulation in roots in BR 27. Interestingly, BR 27 self-grafts and plants having BR 26 rootstock attached to BR 27 scion had no Fe-toxicity induced adverse effect on morphology but showed BR 27 type expressions, confirming that shoot-derived signal triggering Fe-toxicity tolerance in roots. Finally, auxin inhibitor applied with higher Fe concentration caused a significant decline in morpho-physiological parameters along with increased TaSAMS and TaDMAS1 expression in roots of BR 27, revealing the involvement of auxin signaling in response to excess Fe. These findings propose that tolerance to excess Fe in wheat is attributed to the regulation of phytosiderophore limiting Fe acquisition along with increased antioxidant defense in roots driven by shoot-derived auxin signaling.