Abstract
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 Arabidopsis thaliana 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 AtGRXS17 expression were hypersensitive to iron deficiency and showed increased iron concentrations in mature seeds. Disruption of AtGRXS17 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 atgrxs17 mutants to iron deficiency. These findings suggest AtGRXS17 helps integrate redox homeostasis and iron deficiency responses.
Highlights
Iron is an essential mineral nutrient for plants (Guerinot and Yi, 1994; Briat et al, 2015)
ScGrx3 and ScGrx4 play a critical role in iron uptake, trafficking, mitochondrial iron dynamics and homeostasis (Ojeda et al, 2006; Pujol-Carrion et al, 2006; Muhlenhoff et al, 2010)
When expressed in grx3grx4, AtGRXS17 was able to suppress the iron accumulation phenotype of grx3grx4 cells (Figure 1). These results suggest that AtGRXS17 may function in iron regulation in plants
Summary
Iron is an essential mineral nutrient for plants (Guerinot and Yi, 1994; Briat et al, 2015). Studies indicate that adaptation to iron deficiency requires remodeling of the photosynthetic apparatus to minimize the photooxidative damage caused by reactive oxygen species (ROS) (Moseley et al, 2002). Genomewide analyses of both transcript and protein expression profiles reveal significant changes in the expression of genes and/or proteins involved in antioxidant and oxidative stress response pathways (O’Rourke et al, 2007; Forner-Giner et al, 2010; Urzica et al, 2012; Zamboni et al, 2012; Lopez-Millan et al, 2013). The role of ROS and the function of redox-regulatory proteins in iron deficiency response regulation has not been well defined
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