A SRL10-AHP2 signaling module coordinates ROS homeostasis and ion balance for salt stress adaptation in rice.

Soil salinity severely limits crop growth and yield. Deciphering the molecular basis of salt tolerance is thus critical for enhancing food security. We previously identified the SRL10-CATB module in leaf development and thermotolerance. Here, we reveal an additional, essential role for OsSRL10 in salt stress adaptation. OsSRL10 overexpression confers enhanced seedling-stage salt tolerance by promoting ROS scavenging and suppressing Na+ accumulation. Mechanistically, SRL10 physically interacts with the histidine phosphotransfer protein AHP2, a known positive regulator of salt tolerance. Genetic analyses show that the ahp2/srl10 double mutant exhibits salt sensitivity indistinguishable from the srl10 single mutant, and AHP2 overexpression in the srl10 background only partially rescues the phenotype. Together, these results support a model where SRL10 and AHP2 function cooperatively as a functional complex in salt stress adaption. Our study establishes the SRL10-AHP2 module as a key regulatory node in rice salt stress tolerance, serving as a key resource for both understanding stress adaptation and directly improving salt tolerance in rice through breeding.