MicroRNA164d suppresses the HvNAC92-HvHKT1;5 module to enhance salinity tolerance in barley
- Liuhui Kuang
- Hongxing Zhou
- Tongtong Zhang
- Fei Gao
- Tao Yan
- Zhong-Hua Chen
- Qiufang Shen
- Guoping Zhang
- Lin Li
- Dezhi Wu
2025-12-23
Cereal crops (e.g., rice, wheat, maize, and barley) constituted the major component of global human diet and fundamentally changed human society since the dawn of agriculture around 12,000 y ago. Originated and domesticated in different continents and environments, cereal crops vary significantly in their salt tolerance. The High-Affinity K + Transporter1;5s (HKT1;5s) predominately regulate Na + accumulation and salt tolerance in salt-sensitive cereal crops by mediating shoot-to-root Na + exclusion. However, HvHKT1;5 paradoxically promotes root-to-shoot Na + translocation in salt-tolerant barley. Therefore, unravelling the regulatory mechanisms of HvHKT1;5 is critical to understanding the molecular basis of salt tolerance in barley. Here, we demonstrated that a microRNA164d-HvNAC92-HvHKT1;5 module improves salt tolerance via reduced shoot Na + accumulation and increased K + retention in barley, whereas miR164d suppresses HvNAC92 transcription factor to directly downregulate HvHKT1;5 expression. Under salinity condition, the MIR164d -OE, Hvnac92 , and Hvhkt1;5 lines showed significantly reduced root-to-shoot Na + translocation and shoot Na + content compared with the wild-type. In conclusion, we resolve the species-specific function of HKT1;5s in cereal crops by establishing miRNA-guided Na + and K + transport regulation as a regulatory framework for engineering salt-tolerant crops.