Abstract

Iron (Fe) deficiency impairs photosynthetic efficiency, plant growth and biomass yield. This study aimed to reveal the role of nitric oxide (NO) in restoring Fe-homeostasis and oxidative status in Fe-deficient alfalfa. In alfalfa, a shortage of Fe negatively affected the efficiency of root andshoot length, leaf greenness, maximum quantum yield PSII (Fv/Fm), Fe, S, and Zn accumulation, as well as an increase in H2O2 accumulation. In contrast, in the presence of sodium nitroprusside (SNP), a NO donor, these negative effects of Fe deficiency were largely reversed. In response to the SNP, the expression of Fe transporters (IRT1, NRAMP1) and S transporter (SULTR1;2) genes increased in alfalfa. Additionally, the detection of NO generation using fluorescence microscope revealed that SNP treatment increased the level of NO signal, indicating that NO may act as regulatory signal in response to SNP in plants. Interestingly, the increase of antioxidant genes and their related enzymes (Fe-SOD, APX) in response to SNP treatment suggests that Fe-SOD and APX are key contributors to reducing ROS (H2O2) accumulation and oxidative stress in alfalfa. Furthermore, the elevation of Ascorbate-glutathione (AsA-GSH) pathway-related genes (GR and MDAR) Fe-deficiency with SNP implies that the presence of NO relates to enhanced antioxidant defense against Fe-deficiency stress.

Highlights

  • Iron (Fe) is an essential micro-nutrient for plants, as it participates in numerous physiological processes such as photosynthesis, respiration, and nitrogen assimilation [1].any restriction in Fe acquisition hampers plant growth, development, and productivity [2]

  • Iron deficiency-significantly altered the morphological features in alfalfa following

  • Fe deficiency inhibited the growth of alfalfa seedlings compared with those growth was sufficiently stimulated with sodium nitroprusside (SNP) (Figure 1)

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Summary

Introduction

Iron (Fe) is an essential micro-nutrient for plants, as it participates in numerous physiological processes such as photosynthesis, respiration, and nitrogen assimilation [1].any restriction in Fe acquisition hampers plant growth, development, and productivity [2]. In calcareous soils or at high pH levels, Fe is readily oxidized which forms insoluble ferric oxide (Fe3+ ), resulting in Fe (Fe2+ ) deficiency-induced growth inhibition and leaf chlorosis [1]. To deal with this problem, the plant evolved two strategies to deal with soluble Fe (Fe2+ ) shortage and recover Fe from soils. There are strategy-I plants (all dicots and non-graminaceous monocots), in which Fe3+ is reduced into Fe2+ by a plasma membrane ferric reductase enzyme encoded by the FRO (ferric reduction oxidase) gene, before being transported across the rhizodermis cell by a Fe2+ transporter, encoded by an IRT (iron-regulated transporter) gene [1,3].

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