_applied_  
_sciences_  
_Editorial_  
New Molecular Mechanisms of Plant Response to  
Ammonium Nutrition  
**[PERSON] ()**  
State Key Laboratory of Soil and Sustainable Agriculture, Institute of Soil Science, Chinese Academy of Sciences,  
Nanjing 210008, China; [EMAIL_ADDRESS]  
Ammonium (NH4\({}^{+}\)) and nitrate (NO3\({}^{-}\)) are two major inorganic nitrogen (N) forms for plants. In contrast to NH4\({}^{+}\), NO3\({}^{-}\) is highly mobile in soils and is easily leached into groundwater and open water bodies, contributing to eutrophication [1]. Furthermore, NO3\({}^{-}\) must be reduced to NH4\({}^{+}\) in plant cells before it can be utilized by plants in metabolism. This process can consume 12-26% of photosynthetically generated energy [2]. Recent studies have shown that elevated carbon dioxide (CO2) in the atmosphere can inhibit the assimilation of NO3\({}^{-}\) in crop plants and algae, potentially further decreasing the utilization efficiency for NO3\({}^{-}\) in future climates. However, it is puzzling that the theoretically preferred source of Ni is instead toxic to plants [3]. Therefore, it is important to study the molecular mechanisms of plant responses to NH4\({}^{+}\) nutrient stress, and to coordinate NH4\({}^{+}\) uptake and mitigate NH4\({}^{+}\) toxicity. In addition, the effective mitigation of NH4\({}^{+}\) toxicity and improvements in crop NH4\({}^{+}\) tolerance are also crucial for the application of NH4\({}^{+}\)-N fertilizers in agriculture. In recent years, many advances have been made in the study of plant responses to NH4\({}^{+}\) nutrient stress. (i) Which compound, NH4\({}^{+}\) or glutamine (Gln), accumulates and leads to NH4\({}^{+}\) toxicity? High intracellular concentrations of free NH4\({}^{+}\) can lead to NH4\({}^{+}\) toxicity, which may also be exacerbated by metabolic disturbances from excessive NH4\({}^{+}\) assimilation. A recent study indicates that the knockout of _AtGLN2_ enhances tolerance to elevated NH4\({}^{+}\) stress, despite the associated increase in free NH4\({}^{+}\) accumulation [4]. Under high NH4\({}^{+}\) conditions, the reaction of NH4\({}^{+}\) to Gln catalyzed by shoot AtGLN2 produced an abundance of H\({}^{+}\) within the cytosol, thereby inducing acidic stress in shoots. This observation suggests that acidic stress may serve as a principal contributor to NH4\({}^{+}\) toxicity [4]. In rice, mutations in arginininosuccinate lyase (ASL) render the roots more susceptible to NH4\({}^{+}\) stress. Subsequent investigations reveal that ASL mitigates NH4\({}^{+}\) toxicity by promoting the conversion of excess Gln to arginine in the presence of high NH4\({}^{+}\) stress [5]. In summary, the data imply that the metabolic consequences of excess NH4\({}^{+}\), specifically Gln and H\({}^{+}\) accumulation, may pose a greater risk to plants under high NH4\({}^{+}\) stress than the accumulation of free NH4\({}^{+}\) alone. (ii) How do plants modulate NH4\({}^{+}\) uptake in response to elevated NH4\({}^{+}\) concentrations? Optimal regulation of NH4\({}^{+}\) uptake from the environment plays a pivotal role in minimizing intracellular NH4\({}^{+}\) concentrations, thereby alleviating potential NH4\({}^{+}\) toxicity. A previous study has demonstrated that that the protein kinase AtCIPK23 can inhibit NH4\({}^{+}\) uptake through the phosphorylation of a conserved threonine residue located in the C-terminus of AtAMT1;1 and AtAMT1;2 [6]. Subsequent studies have elucidated that the transcription factor AtSTOP1 is capable of directly binding to the _AtCIPK23_ promoter, leading to its transcriptional activation. This, in turn, suppresses the transcription of both _AtAMT1;1_ and _AtAMT1;2_[7]. Furthermore, another protein kinase, AtCIPK15, has been identified to phosphorylate the C-termini of AtAMT1;1, AtAMT1;2, and AtAMT1;3, consequently inhibiting their NH4\({}^{+}\) transport functions [8]. 3. How do phytohormones function in response to NH\({}_{4}\)+ toxicity?