An ICln homolog contributes to osmotic and low‐nitrate tolerance by enhancing nitrate accumulation in Arabidopsis

Nitrate (NO3−) is a source of plant nutrients and osmolytes, but its delivery machineries under osmotic and low‐nutrient stress remain largely unknown. Here, we report that AtICln, an Arabidopsis homolog of the nucleotide‐sensitive chloride‐conductance regulatory protein family (ICln), is involved in response to osmotic and low‐NO3− stress. The gene AtICln, encoding plasma membrane–anchored proteins, was upregulated by various osmotic stresses, and its disruption impaired plant tolerance to osmotic stress. Compared with the wild type, the aticln mutant retained lower anions, particularly NO3−, and its growth retardation was not rescued by NO3− supply under osmotic stress. Interestingly, this mutant also displayed growth defects under low‐NO3 stress, which were accompanied by decreases in NO3− accumulation, suggesting that AtICln may facilitate the NO3− accumulation under NO3− deficiency. Moreover, the low‐NO3− hypersensitive phenotype of aticln mutant was overridden by the overexpression of NRT1.1, an important NO3− transporter in Arabidopsis low‐NO3− responses. Further genetic analysis in the plants with altered activity of AtICln and NRT1.1 indicated that AtICln and NRT1.1 play a compensatory role in maintaining NO3− homeostasis under low‐NO3− environments. These results suggest that AtICln is involved in cellular NO3− accumulation and thus determines osmotic adjustment and low‐NO3− tolerance in plants. Nitrate (NO3−) is an essential component of all life forms, and thus its accumulation in the cytoplasm is fine‐tuned for an optimal NO3− supply under adverse environmental stimuli. We showed that Arabidopsis genome harboured a single homolog of the nucleotide‐sensitive chloride‐conductance regulatory protein family (ICln), referred to as AtICln, that functioned in cytosolic NO3− accumulation for Arabidopsis adaption to osmotic stress and low‐NO3− deficiency. Interestingly, AtICln may partially compensate for the impaired low‐NO3− tolerance induced by defective NRT1.1.