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

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.