The SOS1 transporter of Physcomitrella patens mediates sodium efflux in planta
Article first published online: 2 AUG 2010
© The Authors (2010). Journal compilation © New Phytologist Trust (2010)
Volume 188, Issue 3, pages 750–761, November 2010
How to Cite
Fraile-Escanciano, A., Kamisugi, Y., Cuming, A. C., Rodríguez-Navarro, A. and Benito, B. (2010), The SOS1 transporter of Physcomitrella patens mediates sodium efflux in planta. New Phytologist, 188: 750–761. doi: 10.1111/j.1469-8137.2010.03405.x
- Issue published online: 2 AUG 2010
- Article first published online: 2 AUG 2010
- Received: 17 May 2010Accepted: 22 June 2010
- cell death;
- ENA ATPases;
- Na+ efflux;
- Physcomitrella patens;
- sodium antiporter;
- •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 PpΔsos1 and PpΔena1/PpΔsos1 deletion lines by gene targeting.
- •Comparison of wild-type, and PpΔsos1 and PpΔena1/PpΔsos1 mutant lines revealed that PpSOS1 is crucial for Na+ efflux and that the PpΔsos1 line, and especially the PpΔena1/PpΔsos1 lines, showed excessive Na+ accumulation and Na+-triggered cell death. The PpΔsos1 and PpΔena1/PpΔsos1 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.