The SOS1 transporter of Physcomitrella patens mediates sodium efflux in planta

P>SOS1 is an Na+/H+ antiporter that plays a central role in Na+ tolerance in land plants. SOS1 mediation of Na+ efflux has been studied in plasma-membrane vesicles and deduced from the SOS1 suppression of the Na+ sensitivity of yeast mutants defective in Na+-efflux. However, SOS1-mediated Na+ efflux has not been characterized in either plant or yeast cells. Here, we use Physcomitrella patens to investigate the function of SOS1 in planta. In P. patens, a nonvascular plant in which the study of ion cellular fluxes is technically simple, the existence of two SOS1 genes suggests that the Na+ efflux remaining after the deletion of the ENA1 ATPase is mediated by a SOS1 system. Therefore, we cloned the P. patens SOS1 and SOS1B genes (PpSOS1 and PpSOS1B, respectively) and complementary DNAs, and constructed the Pp Delta sos1 and Pp Delta ena1/Pp Delta sos1 deletion lines by gene targeting. Comparison of wild-type, and Pp Delta sos1 and Pp Delta ena1/Pp Delta sos1 mutant lines revealed that PpSOS1 is crucial for Na+ efflux and that the Pp Delta sos1 line, and especially the Pp Delta ena1/Pp Delta sos1 lines, showed excessive Na+ accumulation and Na+-triggered cell death. The Pp Delta sos1 and Pp Delta ena1/Pp Delta sos1 lines showed impaired high-affinity K+ uptake. Our data support the hypothesis that PpSOS1 mediates cellular Na+ efflux and that PpSOS1 enhances K+ uptake by an indirect effect.