%0 Journal Article
%T Inverse regulation of SOS1 and HKT1 protein localization and stability by SOS3/CBL4 in Arabidopsis thaliana.
%A Gámez-Arjona F
%A Park HJ
%A García E
%A Aman R
%A Villalta I
%A Raddatz N
%A Carranco R
%A Ali A
%A Ali Z
%A Zareen S
%A De Luca A
%A Leidi EO
%A Daniel-Mozo M
%A Xu ZY
%A Albert A
%A Kim WY
%A Pardo JM
%A Sánchez-Rodriguez C
%A Yun DJ
%A Quintero FJ
%J Proc Natl Acad Sci U S A
%V 121
%N 9
%D 2024 Feb 27
%M 38386704
%F 12.779
%R 10.1073/pnas.2320657121
%X To control net sodium (Na+) uptake, Arabidopsis plants utilize the plasma membrane (PM) Na+/H+ antiporter SOS1 to achieve Na+ efflux at the root and Na+ loading into the xylem, and the channel-like HKT1;1 protein that mediates the reverse flux of Na+ unloading off the xylem. Together, these opposing transport systems govern the partition of Na+ within the plant yet they must be finely co-regulated to prevent a futile cycle of xylem loading and unloading. Here, we show that the Arabidopsis SOS3 protein acts as the molecular switch governing these Na+ fluxes by favoring the recruitment of SOS1 to the PM and its subsequent activation by the SOS2/SOS3 kinase complex under salt stress, while commanding HKT1;1 protein degradation upon acute sodic stress. SOS3 achieves this role by direct and SOS2-independent binding to previously unrecognized functional domains of SOS1 and HKT1;1. These results indicate that roots first retain moderate amounts of salts to facilitate osmoregulation, yet when sodicity exceeds a set point, SOS3-dependent HKT1;1 degradation switches the balance toward Na+ export out of the root. Thus, SOS3 functionally links and co-regulates the two major Na+ transport systems operating in vascular plants controlling plant tolerance to salinity.