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

Nitrate (NO ) 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-NO 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 NO , and its growth retardation was not rescued by NO supply under osmotic stress. Interestingly, this mutant also displayed growth defects under low-NO stress, which were accompanied by decreases in NO accumulation, suggesting that AtICln may facilitate the NO accumulation under NO deficiency. Moreover, the low-NO hypersensitive phenotype of aticln mutant was overridden by the overexpression of NRT1.1, an important NO transporter in Arabidopsis low-NO 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 NO homeostasis under low-NO environments. These results suggest that AtICln is involved in cellular NO accumulation and thus determines osmotic adjustment and low-NO tolerance in plants.