Sa Haider

Role of Silicon Counteracting Cadmium Toxicity in Alfalfa (Medicago sativa L.)

Cadmium (Cd) is one of the most phytotoxic elements causing an agricultural problem and human health hazards. This work investigates whether and how silicon (Si) ameliorates Cd toxicity in Alfalfa. The addition of Si in Cd-stressed plants caused significant improvement in morpho-physiological features as well as total protein and membrane stability, indicating that Si does have critical roles in Cd detoxification in Alfalfa. Furthermore, Si supplementation in Cd-stressed plants showed a significant decrease in Cd and Fe concentrations in both roots and shoots compared with Cd-stressed plants, revealing that Si-mediated tolerance to Cd stress is associated with Cd inhibition in Alfalfa. Results also showed no significant changes in the expression of two metal chelators [MsPCS1 (phytochelatin synthase) and MsMT2 (metallothionein)] and PC (phytochelatin) accumulation, indicating that there may be no metal sequestration or change in metal sequestration following Si application under Cd stress in Alfalfa. We further performed a targeted study on the effect of Si on Fe uptake mechanisms. We observed the consistent reduction in Fe reductase activity, expression of Fe-related genes [MsIRT1 (Fe transporter), MsNramp1 (metal transporter) and OsFRO1 (ferric chelate reductase] and Fe chelators (citrate and malate) by Si application to Cd stress in roots of Alfalfa. These results support that limiting Fe uptake through the down-regulation of Fe acquisition mechanisms confers Si-mediated alleviation of Cd toxicity in Alfalfa. Finally, an increase of catalase, ascorbate peroxidase, and superoxide dismutase activities along with elevated methionine and proline subjected to Si application might play roles, at least in part, to reduce H2O2 and to provide antioxidant defense against Cd stress in Alfalfa. The study shows evidence of the effect of Si on alleviating Cd toxicity in Alfalfa and can be further extended for phytoremediation of Cd toxicity in plants.

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

ABSTRACT In this study, zinc (Zn) deficiency caused a significant reduction in growth parameters and tissue Zn concentrations in BRRI 33 (sensitive) but not in Pokkali (tolerant). The increase of proton extrusion in both genotypes under high pH suggests that it gets triggered as a common consequence of reducing pH and solubilization of Zn. Real-time PCR showed pronounced upregulation of OsZIP4, OsDMAS1, OsNAS2 and OsPCS1 in Zn-deficient roots of Pokkali, and to a lesser extent in BRRI 33 only for OsZIP4 and OsPCS1. This suggests that OsDMAS1, OsNAS2 and OsPCS1 functions as secondary consequences leading to higher chelation and uptake of Zn under Zn deficiency in Pokkali. Further, a major increase in CAT, POD, SOD, GR and key metabolites suggests that high antioxidant defense plays a critical role in Zn deficiency tolerance in Pokkali. Further, Pokkali self-grafts and plants having Pokkali rootstock combined with BRRI 33 scion showed no significant decline in plant height, root dry matter and Zn concentration along with upregulation of Zn transporters (OsZIP4 and OsIRT1) under Zn deficiency, suggesting that signal driving mechanisms for Zn deficiency tolerance mechanisms are generated in the root and Zn-inefficient BRRI 33 is not capable of producing signals or sensing them.

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.

Upregulation of OsNAS1, OsPCS1, and DREB1A transcripts along with antioxidative defense confers salt tolerance in rice (Oryza sativa L. cv Pokkali)

ABSTRACT This study investigated the mechanisms associated with differential salt tolerance in two contrasting rice genotypes (Pokkali and BRRI 3). Plant growth, leaf chlorophyll, and Na+ concentrations were significantly affected in BRRI 3 but not in salt-tolerant Pokkali under salt stress. Further, salinity caused upregulation of two chelators named OsNAS1 (nicotianamine synthase) and OsPCS1 (phytochelatin (PC) synthase) along with PC accumulation in roots of Pokkali and BRRI 3, though the expression was more pronounced in Pokkali. It suggests that nicotianamine and PC may chelate excess Na+ under salt stress. Furthermore, greater induction of DREB1A (a transcription factor) in Pokkali suggests that DREB1A may have involvement in salt-induced gene expression in rice. In Pokkali, salt stress caused significant increase in catalase, glutathione reductase, and superoxide dismutase activity only in roots along with enhanced production of glutathione, proline, arginine, methionine, cysteine, serine, and lysine in leaves. These results suggest that Pokkali plants possibly have better protection mechanism against salt-induced oxidative damage due to active antioxidant activities and higher accumulation of glutathione and proline. Taken together, our findings will be useful for transgenic and breeding programs for salt tolerance in rice.