OsNAC10 negatively regulates salt tolerance by repressing OsHKT1;5 expression and reducing shoot-to-root Na⁺...

Maintaining a low sodium (Na⁺) concentration in shoots is a key determinant of 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 governing the transcriptional regulation of HKT1;5 under salt stress remain poorly understood. Here, we identify the rice transcription factor OsNAC10 and characterize its role as a transcriptional repressor of the high-affinity K⁺ transporter gene OsHKT1;5 under salt stress. OsNAC10 expression is predominantly root-localized and is rapidly downregulated in response to salt treatment. OsNAC10 knockout mutants exhibit enhanced salt tolerance, reduced shoot Na⁺ accumulation, and decreased root-to-shoot Na⁺ transport, whereas overexpression lines show increased Na⁺ accumulation and pronounced salt sensitivity. Subcellular localization and molecular interaction analyses reveal 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 is markedly upregulated in nac10 mutants under salt stress. Genetic analysis further demonstrates that the enhanced salt tolerance of the nac10 mutant depends on OsHKT1;5, as the nac10 hkt1;5 double mutant exhibits a salt-sensitive phenotype comparable to that of the hkt1;5 single mutant. Importantly, under saline soil conditions, OsNAC10 knockout lines maintain significantly higher grain yield than wild-type plants. Together, these findings uncover a novel transcriptional regulatory mechanism in which OsNAC10 negatively modulates rice salt tolerance by competitively inhibiting OsHKT1;5 expression, highlighting OsNAC10 as a promising target for breeding salt-tolerant crops.