miR5810-OsMRLP6 module regulates rice salt tolerance by affecting ROS accumulation and K⁺/Na⁺ homeostasis

Soil salinity poses a major threat to rice production. It is well-established that microRNAs (miRNAs) function as pivotal regulators in mediating plant responses to abiotic stress. The miR5810-OsMRLP6 module has previously been shown to regulate rice yield by modulating photosynthesis. However, whether miR5810 is involved in salt stress response remained unclear. In this study, we found that salt stress induced miR5810 expression but conversely suppressed OsMRLP6 expression. Genetic evidence showed that both miR5810-knockdown (STTM5810) and OsMRLP6-overexpressing (MRLP6-ox) plants exhibited enhanced salt tolerance, with higher survival rates, increased chlorophyll content, and greater fresh weight. In contrast, miR5810-overexpressing (miR5810-ox) and OsMRLP6-knockout (mrlp6-ko) plants displayed opposite phenotypes. Consistently, reverse transcription quantitative PCR assays revealed that STTM5810 and MRLP6-ox plants upregulated genes involved in K⁺/Na⁺ transport and oxidative stress responses under salt treatment. Physiological analyses further showed that STTM5810 and MRLP6-ox plants alleviated salt-induced oxidative damage by enhancing ROS scavenging capacity and promoting K⁺/Na⁺ homeostasis. Furthermore, salt stress assays using the ROS scavenger N-acetylcysteine (NAC) suggested that miR5810-OsMRLP6 module functions in an ROS-mediated salt signaling pathway. Taken together, our results indicate that miR5810-OsMRLP6 module regulates rice salt tolerance by modulating ROS accumulation and K⁺/Na⁺ homeostasis. These findings highlight a dual-benefit strategy with significant translational potential for improving salt tolerance and productivity in rice.