Induction of S-nitrosoglutathione reductase protects root growth from ammonium toxicity by regulating potassium homeostasis in Arabidopsis and rice

Author:

Zhang Lin1,Song Haiyan2,Li Baohai3,Wang Meng1,Di Dongwei1,Lin Xianyong3,Kronzucker Herbert J45,Shi Weiming1ORCID,Li Guangjie1ORCID

Affiliation:

1. State Key Laboratory of Soil and Sustainable Agriculture, Institute of Soil Science, Chinese Academy of Sciences, Nanjing, China

2. Academic Affairs Office, Foshan University, Foshan, China

3. MOE Key Laboratory of Environment Remediation and Ecological Health, College of Environmental & Resource Sciences, Zhejiang University, HangzhouChina

4. Faculty of Land and Food Systems, University of British Columbia, Vancouver, BC, Canada

5. School of BioSciences, The University of Melbourne, Parkville, Victoria, Australia

Abstract

Abstract Ammonium (NH4+) is toxic to root growth in most plants already at moderate levels of supply, but mechanisms of root growth tolerance to NH4+ remain poorly understood. Here, we report that high levels of NH4+ induce nitric oxide (NO) accumulation, while inhibiting potassium (K+) acquisition via SNO1 (sensitive to nitric oxide 1)/SOS4 (salt overly sensitive 4), leading to the arrest of primary root growth. High levels of NH4+ also stimulated the accumulation of GSNOR (S-nitrosoglutathione reductase) in roots. GSNOR overexpression improved root tolerance to NH4+. Loss of GSNOR further induced NO accumulation, increased SNO1/SOS4 activity, and reduced K+ levels in root tissue, enhancing root growth sensitivity to NH4+. Moreover, the GSNOR-like gene, OsGSNOR, is also required for NH4+ tolerance in rice. Immunoblotting showed that the NH4+-induced GSNOR protein accumulation was abolished in the VTC1- (vitamin C1) defective mutant vtc1-1, which is hypersensititive to NH4+ toxicity. GSNOR overexpression enhanced vtc1-1 root tolerance to NH4+. Our findings suggest that induction of GSNOR increases NH4+ tolerance in Arabidopsis roots by counteracting NO-mediated suppression of tissue K+, which depends on VTC1 function.

Funder

National Key R&D Program of China

National Natural Science Foundation of China

Natural Science Foundation of Jiangsu Province

University of Melbourne

Publisher

Oxford University Press (OUP)

Subject

Plant Science,Physiology

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