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Nat Commun. 2019 Aug 29;10(1):3896. doi: 10.1038/s41467-019-11892-5.

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

Li B1,2,3,4, Sun L5, Huang J6,7, Göschl C8, Shi W5, Chory J6,7, Busch W9,10,11.

Author information

1
College of Environmental and Resource Sciences, Zhejiang University, 866 Yuhangtang Road, Hangzhou, Zhejiang, 310058, China. 0019054@zju.edu.cn.
2
Plant Biology Laboratory, Salk Institute for Biological Studies, 10010 N Torrey Pines Rd, La Jolla, CA, 92037, USA. 0019054@zju.edu.cn.
3
Integrative Biology Laboratory, Salk Institute for Biological Studies, 10010 N Torrey Pines Rd, La Jolla, CA, 92037, USA. 0019054@zju.edu.cn.
4
Gregor Mendel Institute (GMI), Austrian Academy of Sciences, Vienna Biocenter (VBC), Dr Bohr-Gasse 3, 1030, Vienna, Austria. 0019054@zju.edu.cn.
5
State Key Laboratory of Soil and Sustainable Agriculture, Institute of Soil Science, Chinese Academy of Sciences, No. 71 East Beijing Road, Nanjing, 210008, China.
6
Plant Biology Laboratory, Salk Institute for Biological Studies, 10010 N Torrey Pines Rd, La Jolla, CA, 92037, USA.
7
Howard Hughes Medical Institute, Salk Institute for Biological Studies, La Jolla, CA, 92037, USA.
8
Gregor Mendel Institute (GMI), Austrian Academy of Sciences, Vienna Biocenter (VBC), Dr Bohr-Gasse 3, 1030, Vienna, Austria.
9
Plant Biology Laboratory, Salk Institute for Biological Studies, 10010 N Torrey Pines Rd, La Jolla, CA, 92037, USA. wbusch@salk.edu.
10
Integrative Biology Laboratory, Salk Institute for Biological Studies, 10010 N Torrey Pines Rd, La Jolla, CA, 92037, USA. wbusch@salk.edu.
11
Gregor Mendel Institute (GMI), Austrian Academy of Sciences, Vienna Biocenter (VBC), Dr Bohr-Gasse 3, 1030, Vienna, Austria. wbusch@salk.edu.

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.

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