GSNOR provides plant tolerance to iron toxicity via preventing iron-dependent nitrosative and oxidative cytotoxicity

Baohai Li (), Li Sun, Jianyan Huang, Christian Göschl, Weiming Shi, Joanne Chory and Wolfgang Busch ()
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Baohai Li: Zhejiang University
Li Sun: Chinese Academy of Sciences
Jianyan Huang: Salk Institute for Biological Studies
Christian Göschl: Vienna Biocenter (VBC)
Weiming Shi: Chinese Academy of Sciences
Joanne Chory: Salk Institute for Biological Studies
Wolfgang Busch: Salk Institute for Biological Studies

Nature Communications, 2019, vol. 10, issue 1, 1-13

Abstract: Abstract Iron (Fe) is essential for life, but in excess can cause oxidative cytotoxicity through the generation of Fe-catalyzed reactive oxygen species. It is yet unknown which genes and mechanisms can provide Fe-toxicity tolerance. Here, we identify S-nitrosoglutathione-reductase (GSNOR) variants underlying a major quantitative locus for root tolerance to Fe-toxicity in Arabidopsis using genome-wide association studies and allelic complementation. These variants act largely through transcript level regulation. We further show that the elevated nitric oxide is essential for Fe-dependent redox toxicity. GSNOR maintains root meristem activity and prevents cell death via inhibiting Fe-dependent nitrosative and oxidative cytotoxicity. GSNOR is also required for root tolerance to Fe-toxicity throughout higher plants such as legumes and monocots, which exposes an opportunity to address crop production under high-Fe conditions using natural GSNOR variants. Overall, this study shows that genetic or chemical modulation of the nitric oxide pathway can broadly modify Fe-toxicity tolerance.

Date: 2019
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DOI: 10.1038/s41467-019-11892-5

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