The Arabidopsis AMOT1/EIN3 gene plays an important role in the amelioration of ammonium toxicity

Ammonium (NH(4)(+)) toxicity inhibits shoot growth in Arabidopsis, but the underlying mechanisms remain poorly characterized. Here, we show that a novel Arabidopsis mutant, ammonium tolerance 1 (amot1), exhibits enhanced shoot growth tolerance to NH(4)(+). Molecular cloning revealed that amot1 is a new allele of EIN3, a key regulator of ethylene responses. The amot1 mutant and the allelic ein3-1 mutants show greater NH(4)(+) tolerance than the wild type. Moreover, transgenic plants overexpressing EIN3 (EIN3ox) are more sensitive to NH(4)(+) toxicity The ethylene precursor 1-aminocyclopropane-1-carboxylic acid (ACC) increases shoot sensitivity to NH(4)(+), whereas the ethylene perception inhibitor Ag(+) decreases sensitivity. NH(4)(+) induces ACC and ethylene accumulation. Furthermore, ethylene-insensitive mutants such as etr1-3 and ein3eil1 display enhanced NH(4)(+) tolerance. In contrast, the ethylene overproduction mutant eto1-1 exhibits decreased ammonium tolerance. AMOT1/EIN3 positively regulates shoot ROS accumulation, leading to oxidative stress under NH(4)(+) stress, a trait that may be related to increased expression of peroxidase-encoding genes. These findings demonstrate the role of AMOT1/EIN3 in NH(4)(+) tolerance and confirm the strong link between NH(4)(+) toxicity symptoms and the accumulation of hydrogen peroxide.