ABSTRACT Iron (Fe) is a mineral nutrient and a metal cofactor essential for plants. Iron limitation can have detrimental effects on plant growth and development, while excess iron inside plant cells leads to oxidative damage. As a result, plants have evolved complex regulatory networks to respond to fluctuations in cellular iron concentrations. The mechanisms that regulate these responses however, are not fully understood. Heterologous expression of an Arabidopsis thaliana monothiol glutaredoxin S17 (GRXS17) suppresses the over-accumulation of iron in the Saccharomyces cerevisiae Grx3/Grx4 mutant and disruption of GRXS17 causes plant sensitivity to exogenous oxidants and iron deficiency stress. GRXS17 may act as an important regulator in the plant’s ability to respond to iron deficiency stress and maintain redox homeostasis. Here, we extend this investigation by analyzing iron-responsive gene expression of the Fer-like iron deficiency-induced transcription factor (FIT) network (FIT, IRT1, FRO1, and FRO2) and the bHLH transcription factor POPEYE (PYE) network (PYE, ZIF1, FRO3, NAS4, and BTS) in GRXS17 KO plants and wildtype controls grown under iron sufficiency and deficiency conditions. Our findings suggest that GRXS17 is required for tolerance to iron deficiency, and plays a negative regulatory role under conditions of iron sufficiency.

中文翻译：

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拟南芥谷氧还蛋白S17功能丧失植物铁响应基因表达的改变有无铁胁迫

摘要 铁 (Fe) 是一种矿物质营养素和植物必需的金属辅助因子。铁限制会对植物生长和发育产生不利影响，而植物细胞内过量的铁会导致氧化损伤。因此，植物已经进化出复杂的调节网络来响应细胞铁浓度的波动。然而，调节这些反应的机制尚不完全清楚。拟南芥单硫醇谷氧还蛋白 S17 (GRXS17) 的异源表达抑制了酿酒酵母 Grx3/Grx4 突变体中铁的过度积累，并且 GRXS17 的破坏导致植物对外源性氧化剂和缺铁胁迫敏感。GRXS17 可能是植物响应缺铁胁迫和维持氧化还原稳态的能力的重要调节剂。这里，我们通过分析 Fer 样缺铁诱导转录因子 (FIT) 网络（FIT、IRT1、FRO1 和 FRO2）和 bHLH 转录因子 POPEYE（PYE）网络（PYE、ZIF1）的铁响应基因表达来扩展这项研究、FRO3、NAS4 和 BTS）在 GRXS17 KO 植物和在铁充足和缺铁条件下生长的野生型对照中。我们的研究结果表明 GRXS17 是对缺铁的耐受所必需的，并且在铁充足的条件下发挥负调节作用。和 BTS）在 GRXS17 KO 植物和在铁充足和缺铁条件下生长的野生型对照中。我们的研究结果表明 GRXS17 是对缺铁的耐受所必需的，并且在铁充足的条件下发挥负调节作用。和 BTS）在 GRXS17 KO 植物和在铁充足和缺铁条件下生长的野生型对照中。我们的研究结果表明 GRXS17 是对缺铁的耐受所必需的，并且在铁充足的条件下发挥负调节作用。