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.

The plant hormone, abscisic acid (ABA), is not only important for promoting abiotic stress responses but also plays a versatile and crucial role in plant immunity. The pathogen infection-induced dynamic accumulation of ABA mediates the degradation of non-expresser of PR genes 1 (NPR1) through the CUL3^NPR3NPR4 proteasome pathway. However, the functional significance of NPR1 degradation by other E3 ligases in response to ABA remains unclear. Here, we report that NPR1 is induced transcriptionally by ABA and that npr1-1 mutation results in ABA insensitivity during seed germination and seedling growth. Mutants lacking NPR1 downregulate the expression of ABA-responsive transcription factors ABA INSENSITIVE4 (ABI4) and ABA INSENSITIVE5 (ABI5), and that of their downstream targets EM6, RAB18, RD26, and RD29B. The npr1-1 mutation also affects the transcriptional activity of WRKY18, which activates WRKY60 in the presence of ABA. Furthermore, NPR1 directly interacts with and is degraded by HOS15, a substrate receptor for the DDB1-CUL4 ubiquitin E3 ligase complex. Collectively, our findings demonstrate that NPR1 acts as a positive regulator of ABA-responsive genes, whereas HOS15 promotes NPR1 degradation in a proteasome-dependent manner.

Salt stress is a major abiotic factor that limits plant productivity. Plants have evolved sophisticated signaling networks to resist salinity, with the salt overly sensitive (SOS) pathway playing a central role in maintaining ion homeostasis. In this pathway, the calcium-binding protein SOS3 (CBL4) acts as a primary calcium sensor, translating transient cytosolic Ca²⁺ signals into phosphorylation cascades that regulate Na⁺ extrusion and K⁺ retention. In addition to its role in salt stress, SOS3 influences diverse developmental processes, including root and shoot architecture, flowering time, and seed germination, through crosstalk with several signaling pathways, such as abscisic acid, reactive oxygen species, and MAPKs. SOS3 also promotes the activation of SOS1 and negatively regulates the protein stability of HKT1, two key Na⁺ transport systems in roots and shoots. Recent advances in Arabidopsis and major crops, such as rice, tomato, and cotton, have deepened our understanding of the SOS3 regulatory network, paving the way for the engineering of salt-tolerant cultivars. In this review, we summarize current insights into SOS3-mediated signaling, emphasizing its dual roles in plant development and adaptive stress responses, and discuss future directions for enhancing crop resilience through manipulation of SOS3 signaling.