LAUSR

Abstract Although several literatures confirmed the beneficial roles of exogenous melatonin in the enhancement of salinity tolerance in plants, whether or how endogenous melatonin confers plant salinity tolerance is still elusive. In the report, we observed impaired melatonin level and salinity hypersensitivity in atsnat, the Arabidopsis melatonin synthesis mutant. Above hypersensitivity was rescued by melatonin or hydrogen peroxide. Meanwhile, melatonin‐mediated salt tolerance in wild‐type was abolished by an NADPH oxidase inhibitor, suggesting the possible role of NADPH oxidase‐dependent reactive oxygen species (ROS). Genetic evidence further showed that the rapid stimulated RbohF transcripts and production of ROS elicited by melatonin in stressed wild‐type plants were largely abolished by the mutation of AtrbohF. Meanwhile, salinity sensitivity of atrbohF mutant was not altered by melatonin, which was consistent with the higher Na+ content and the resulting greater Na+/K+ ratio, compared with those in wild‐type plants. Further changes of SOS1, SOS2, and SOS3 transcripts suggested that the melatonin‐triggered SOS‐mediated Na+ efflux might be mediated by AtrbohF‐dependent ROS. The addition of melatonin could intensify the increased antioxidant defence in stressed wild‐type but not in atrbohF mutant, both of which were confirmed by the histochemical staining for ROS production and lipid peroxidation during the later period of stress. Collectively, our genetic and molecular evidence revealed that the AtrbohF‐dependent ROS signaling is required for melatonin‐induced salinity tolerance via the reestablishment of ion and redox homeostasis. Graphical abstract Figure. No Caption available. HighlightsSalt hypersensitivity of atsnat mutant is rescued by melatonin and H2O2.Melatonin‐mediated salt tolerance is sensitive to DPI, an inhibitor of NADPH oxidase.AtrbohF is required for melatonin‐induced salinity tolerance.Ion homeostasis and redox homeostasis are reestablished by melatonin via AtrbohF.