Abstract
The wheat sodium transporters TmHKT1;5-A and TaHKT1;5-D are encoded by genes underlying major shoot Na+ exclusion loci Nax2 and Kna1 from Triticum monococcum (Tm) and Triticum aestivum (Ta), respectively. In contrast to HKT2 transporters that have been shown to exhibit high affinity K+-dependent Na+ transport, HKT1 proteins have, with one exception, only been shown to catalyse low affinity Na+ transport and no K+ transport. Here, using heterologous expression in Xenopus laevis oocytes we show that both TmHKT1;5-A and TaHKT1;5-D encode dual (high and low) affinity Na+-transporters with the high-affinity component being abolished when external K+ is in excess of external Na+. The low-affinity component for Na+ transport of TmHKT1;5-A had a lower Km than that of TaHKT1;5-D even when blocked by external K+. We use 3-D structural modelling to explain how K+ block may occur and propose potential physiological consequences of K+ block. The transport properties and localisation of wheat HKT1;5 proteins are well suited for their role in a ‘gatekeeper’ process that secure shoot Na+-exclusion and underpin recent advances for improving crop plant salt tolerance.