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An ICln homolog contributes to osmotic and low‐nitrate tolerance by enhancing nitrate accumulation in Arabidopsis
Author(s) -
Chu Moli,
Wang Yuan,
Mu Baicong,
Ge Haiman,
Zhang Chi,
Zhao Fugeng,
Fu Aigen,
Luan Sheng,
Li Legong,
Lan Wenzhi
Publication year - 2021
Publication title -
plant, cell and environment
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.646
H-Index - 200
eISSN - 1365-3040
pISSN - 0140-7791
DOI - 10.1111/pce.14005
Subject(s) - arabidopsis , nitrate , chemistry , biophysics , biochemistry , biology , organic chemistry , mutant , gene
Abstract Nitrate (NO 3 − ) 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 3 − 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 3 − , and its growth retardation was not rescued by NO 3 − supply under osmotic stress. Interestingly, this mutant also displayed growth defects under low‐NO 3 stress, which were accompanied by decreases in NO 3 − accumulation, suggesting that AtICln may facilitate the NO 3 − accumulation under NO 3 − deficiency. Moreover, the low‐NO 3 − hypersensitive phenotype of aticln mutant was overridden by the overexpression of NRT1.1, an important NO 3 − transporter in Arabidopsis low‐NO 3 − 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 3 − homeostasis under low‐NO 3 − environments. These results suggest that AtICln is involved in cellular NO 3 − accumulation and thus determines osmotic adjustment and low‐NO 3 − tolerance in plants.