AI Article Synopsis

  • Arabidopsis plants use the SOS1 Na/H antiporter and HKT1;1 protein to manage sodium uptake and unloading, balancing Na levels within the plant.
  • The SOS3 protein serves as a molecular switch that enhances SOS1 activity for Na export while facilitating degradation of HKT1;1 under high salt conditions.
  • This co-regulation by SOS3 helps plants maintain salt balance for osmoregulation and enhances their tolerance to saline environments.

Article Abstract

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.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10907282PMC
http://dx.doi.org/10.1073/pnas.2320657121DOI Listing

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