Salicylic acid improves salinity tolerance in Arabidopsis by restoring membrane potential and preventing salt-induced K+ loss via a GORK channel.

Despite numerous reports implicating salicylic acid (SA) in plant salinity responses, the specific ionic mechanisms of SA-mediated adaptation to salt stress remain elusive. To address this issue, a non-invasive microelectrode ion flux estimation technique was used to study kinetics of NaCl-induced net ion fluxes in Arabidopsis thaliana in response to various SA concentrations and incubation times. NaCl-induced K(+) efflux and H(+) influx from the mature root zone were both significantly decreased in roots pretreated with 10-500 μM SA, with strongest effect being observed in the 10-50 μM SA range. Considering temporal dynamics (0-8-h SA pretreatment), the 1-h pretreatment was most effective in enhancing K(+) retention in the cytosol. The pharmacological, membrane potential, and shoot K(+) and Na(+) accumulation data were all consistent with the model in which the SA pretreatment enhanced activity of H(+)-ATPase, decreased NaCl-induced membrane depolarization, and minimized NaCl-induced K(+) leakage from the cell within the first hour of salt stress. In long-term treatments, SA increased shoot K(+) and decreased shoot Na(+) accumulation. The short-term NaCl-induced K(+) efflux was smallest in the gork1-1 mutant, followed by the rbohD mutant, and was highest in the wild type. Most significantly, the SA pretreatment decreased the NaCl-induced K(+) efflux from rbohD and the wild type to the level of gork1-1, whereas no effect was observed in gork1-1. These data provide the first direct evidence that the SA pretreatment ameliorates salinity stress by counteracting NaCl-induced membrane depolarization and by decreasing K(+) efflux via GORK channels.