Yu Han, Yang Jian, Shi Yafei, Donelson Jimmonique, Thompson Sean M, Sprague Stuart, Roshan Tony, Wang Da-Li, Liu Jianzhong, Park Sunghun, Nakata Paul A, Connolly Erin L, Hirschi Kendal D, Grusak Michael A, Cheng Ninghui
USDA/ARS Children's Nutrition Research Center, Department of Pediatrics, Baylor College of Medicine, HoustonTX, United States.
College of Chemistry and Life Science, Zhejiang Normal UniversityJinhua, China.
Front Plant Sci. 2017 Jun 19;8:1045. doi: 10.3389/fpls.2017.01045. eCollection 2017.
Iron (Fe) is an essential mineral nutrient and a metal cofactor required for many proteins and enzymes involved in the processes of DNA synthesis, respiration, and photosynthesis. Iron limitation can have detrimental effects on plant growth and development. Such effects are mediated, at least in part, through the generation of reactive oxygen species (ROS). Thus, plants have evolved a complex regulatory network to respond to conditions of iron limitations. However, the mechanisms that couple iron deficiency and oxidative stress responses are not fully understood. Here, we report the discovery that an monothiol glutaredoxin S17 (AtGRXS17) plays a critical role in the plants ability to respond to iron deficiency stress and maintain redox homeostasis. In a yeast expression assay, AtGRXS17 was able to suppress the iron accumulation in yeast ScGrx3/ScGrx4 mutant cells. Genetic analysis indicated that plants with reduced expression were hypersensitive to iron deficiency and showed increased iron concentrations in mature seeds. Disruption of caused plant sensitivity to exogenous oxidants and increased ROS production under iron deficiency. Addition of reduced glutathione rescued the growth and alleviates the sensitivity of mutants to iron deficiency. These findings suggest AtGRXS17 helps integrate redox homeostasis and iron deficiency responses.
铁(Fe)是一种必需的矿物质营养素,也是许多参与DNA合成、呼吸作用和光合作用过程的蛋白质及酶所需的金属辅因子。铁限制会对植物生长发育产生不利影响。这种影响至少部分是通过活性氧(ROS)的产生介导的。因此,植物进化出了一个复杂的调控网络来应对铁限制条件。然而,将铁缺乏与氧化应激反应联系起来的机制尚未完全了解。在此,我们报告发现单硫醇谷氧还蛋白S17(AtGRXS17)在植物对铁缺乏胁迫的反应及维持氧化还原稳态的能力中起关键作用。在酵母表达试验中,AtGRXS17能够抑制酵母ScGrx3/ScGrx4突变细胞中的铁积累。遗传分析表明,表达降低的植物对铁缺乏高度敏感,且成熟种子中的铁浓度增加。AtGRXS17的缺失导致植物对外源氧化剂敏感,并在铁缺乏条件下增加ROS产生。添加还原型谷胱甘肽可挽救生长并减轻AtGRXS17突变体对铁缺乏的敏感性。这些发现表明AtGRXS17有助于整合氧化还原稳态和铁缺乏反应。