Isolation and characterization of a novel ammonium overly sensitive mutant, amos2, in Arabidopsis thaliana

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.