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Inverse regulation of SOS1 and HKT1 protein localization and stability by SOS3/CBL4 in Arabidopsis thaliana

2024; National Academy of Sciences; Volume: 121; Issue: 9 Linguagem: Inglês

10.1073/pnas.2320657121

1091-6490

Francisco M. Gámez‐Arjona, Hee Jin Park, Elena González, Rashid Aman, Irène Villalta, Natalia Raddatz, Raúl Carranco, Akhtar Ali, Zahir Ali, Shah Zareen, Anna Irene De Luca, Eduardo O. Leidi, Miguel Daniel-Mozo, Zheng‐Yi Xu, Armando Albert, Woe‐Yeon Kim, José M. Pardo, Clara Sánchez‐Rodríguez, Dae‐Jin Yun, Francisco J. Quintero,

Plant Molecular Biology Research

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.