Molecular hydrogen-induced salinity tolerance requires melatonin signalling in Arabidopsis thaliana

Abstract

Melatonin (MT) plays positive roles in salinity stress tolerance. However, the upstream signalling components that regulate MT are poorly understood. Here, we report that endogenous MT acts downstream of molecular hydrogen (H₂ ) in the salinity response in Arabidopsis. The addition of hydrogen-rich water and expression of the hydrogenase1 gene (CrHYD1) from Chlamydomonas reinhardtii increased endogenous H₂ and MT levels and enhanced salinity tolerance. These results were not observed in the absence of serotonin N-acetyltransferase gene (SNAT). H₂ increased the levels of SNAT transcripts in the wild-type and CrHYD1 lines, which had lower Na⁺ /K⁺ ratios and higher levels of ion transport-related gene transcripts. These changes were not observed in atsnat/CrHYD1-4 hybrids. The increased MT-dependent Na⁺ extrusion observed in the CrHYD1 plants resulted, at least in part, from enhanced Na⁺ /H⁺ antiport across the plasma membrane. The endogenous H₂ -induced MT-dependent regulation of ion and redox homeostasis was impaired in the atsnat/CrHYD1-4 hybrids. Taken together, these results demonstrate that MT-induced salinity tolerance is induced by a H₂ signalling cascade that regulates ion and redox homeostasis in response to salinity.

Keywords: endogenous H2; serotonin N-acetyltransferase.