Isolation and characterization of a novel ammonium overly sensitive mutant, amos2, in Arabidopsis thaliana
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- 作者：Guangjie Li (1) (2)
Gangqiang Dong (1) (2)
Baohai Li (1)
Qing Li (1)
Herbert J. Kronzucker (3)
Weiming Shi (1) - 关键词：Ammonium toxicity ; amos2 mutant ; Arabidopsis ; Cation homeostasis ; Genetic mapping ; Potassium
- 刊名：Planta
- 出版年：2012
- 出版时间：February 2012
- 年：2012
- 卷：235
- 期：2
- 页码：239-252
- 全文大小：865KB
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Gangqiang Dong (1) (2)
Baohai Li (1)
Qing Li (1)
Herbert J. Kronzucker (3)
Weiming Shi (1)
1. State Key Laboratory of Soil and Sustainable Agriculture, Institute of Soil Science, Chinese Academy of Sciences, No.71 East Beijing Road, Nanjing, 210008, China
2. Graduate School of Chinese Academy of Science, Beijing, 100081, China
3. Department of Biological Sciences, University of Toronto, 1265 Military Trail, Toronto, ON, M1C 1A4, Canada
文摘
Ammonium (NH4 +) toxicity is a significant agricultural problem globally, compromising crop growth and productivity in many areas. However, the molecular mechanisms of NH4 + toxicity are still poorly understood, in part due to a lack of valuable genetic resources. Here, a novel Arabidopsis mutant, amos2 (ammonium overly sensitive 2), displaying hypersensitivity to NH4 + in both shoots and roots, was isolated. The mutant exhibits the hallmarks of NH4 + toxicity at significantly elevated levels: severely suppressed shoot biomass, increased leaf chlorosis, and inhibition of lateral root formation. Amos2 hypersensitivity is associated with excessive NH4 + accumulation in shoots and a reduction in tissue potassium (K+), calcium (Ca2+), and magnesium (Mg2+). We show that the lesion is specific to the NH4 + ion, is independent of NH4 + metabolism, and can be partially rescued by elevated external K+. The amos2 lesion was mapped to a 16-cM interval on top of chromosome 1, where no similar mutation has been previously mapped. Our study identifies a novel locus controlling cation homeostasis under NH4 + stress and provides a tool for the future identification of critical genes involved in the development of NH4 + toxicity.