OsNAC10 negatively regulates salt tolerance by repressing the expression of OsHKT1;5 and reducing recirculation of Na+ from shoots to roots in rice

Maintaining low sodium (Na+) concentration in shoots is a key strategy determining salt tolerance in cereal crops. This process is largely mediated by Na+ transporters such as HKT1;5, which controls long-distance Na+ transport; however, the molecular mechanisms underlying the transcriptional regulation of HKT1;5 under salt stress remain poorly understood. Here, we identified a rice transcription factor gene, OsNAC10, and characterized its function as a transcriptional repressor of the high-affinity K+ transporter gene OsHKT1;5 under salt stress. OsNAC10 expression was root-predominant and rapidly down-regulated by salt stress. OsNAC10 knock-out mutants exhibited enhanced salt tolerance, lower shoot Na+ concentration, and reduced root-to-shoot Na+ transportation, whereas its overexpression lines showed increased Na+ accumulation and pronounced salt sensitivity. Subcellular localization and molecular interaction analyses revealed that OsNAC10 is a nuclear-localized transcription factor that directly and competitively binds to an ACGTA-core cis-element within the OsHKT1;5 promoter. Consequently, OsHKT1;5 expression was markedly up-regulated in nac10 mutants under salt stress. Genetic analysis demonstrated that the enhanced salt tolerance of the nac10 mutant was dependent on OsHKT1;5, as the nac10/hkt1;5 double mutant exhibited a salt-sensitive phenotype comparable to that of the hkt1;5 single mutant. Importantly, under saline soil conditions, OsNAC10 knockout lines maintained significantly higher grain yield relative to wild-type plants. Our findings reveal a novel transcriptional regulatory mechanism in which OsNAC10 negatively modulates rice salt tolerance by competitively inhibiting OsHKT1;5 expression, highlighting its potential as a promising target for breeding salt-tolerant crops.