Calcium is a universal secondary messenger that triggers many cellular responses. However, it is unclear how a calcium signal is coordinately decoded by different calcium sensors, which in turn regulate downstream targets to fulfill a specific physiological function. Here we show that SOS2-LIKE PROTEIN KINASE5 (PKS5) can negatively regulate the Salt-Overly-Sensitive signaling pathway in Arabidopsis. PKS5 can interact with and phosphorylate SOS2 at Ser²⁹⁴, promote the interaction between SOS2 and 14-3-3 proteins, and repress SOS2 activity. However, salt stress promotes an interaction between 14-3-3 proteins and PKS5, repressing its kinase activity and releasing inhibition of SOS2. We provide evidence that 14-3-3 proteins bind to Ca²⁺, and that Ca²⁺ modulates 14-3-3-dependent regulation of SOS2 and PKS5 kinase activity. Our results suggest that a salt-induced calcium signal is decoded by 14-3-3 and SOS3/SCaBP8 proteins, which selectively activate/inactivate the downstream protein kinases SOS2 and PKS5 to regulate Na⁺ homeostasis by coordinately mediating plasma membrane Na⁺/H⁺ antiporter and H⁺-ATPase activity.

Saline-alkali soil is a major environmental constraint impairing plant growth and crop productivity. In this study, we identified a Ca²⁺ sensor/kinase/plasma membrane (PM) H⁺-ATPase module as a central component conferring alkali tolerance in Arabidopsis (Arabidopsis thaliana). We report that the SCaBP3 (SOS3-LIKE CALCIUM BINDING PROTEIN3)/CBL7 (CALCINEURIN B-LIKE7) loss-of-function plants exhibit enhanced stress tolerance associated with increased PM H⁺-ATPase activity and provide fundamental mechanistic insights into the regulation of PM H⁺-ATPase activity. Consistent with the genetic evidence, interaction analyses, in vivo reconstitution experiments, and determination of H⁺-ATPase activity indicate that interaction of the Ca²⁺ sensor SCaBP3 with the C-terminal Region I domain of the PM H⁺-ATPase AHA2 (Arabidopsis thaliana PLASMA MEMBRANE PROTON ATPASE2) facilitates the intramolecular interaction of the AHA2 C terminus with the Central loop region of the PM H⁺-ATPase to promote autoinhibition of H⁺-ATPase activity. Concurrently, direct interaction of SCaPB3 with the kinase PKS5 (PROTEIN KINASE SOS2-LIKE5) stabilizes the kinase-ATPase interaction and thereby fosters the inhibitory phosphorylation of AHA2 by PKS5. Consistently, yeast reconstitution experiments and genetic analysis indicate that SCaBP3 provides a bifurcated pathway for coordinating intramolecular and intermolecular inhibition of PM H⁺-ATPase. We propose that alkaline stress-triggered Ca²⁺ signals induce SCaBP3 dissociation from AHA2 to enhance PM H⁺-ATPase activity. This work illustrates a versatile signaling module that enables the stress-responsive adjustment of plasma membrane proton fluxes.

Soil salinization inhibits plant growth and seriously restricts food security and agricultural development. Excessive salt can cause ionic stress, osmotic stress, and ultimately oxidative stress in plants. Plants exclude excess salt from their cells to help maintain ionic homeostasis and stimulate phytohormone signaling pathways, thereby balancing growth and stress tolerance to enhance their survival. Continuous innovations in scientific research techniques have allowed great strides in understanding how plants actively resist salt stress. Here, we briefly summarize recent achievements in elucidating ionic homeostasis, osmotic stress regulation, oxidative stress regulation, and plant hormonal responses under salt stress. Such achievements lay the foundation for a comprehensive understanding of plant salt-tolerance mechanisms.

Saline-alkali soils pose an increasingly serious global threat to plant growth and productivity. Much progress has been made in elucidating how plants adapt to salt stress by modulating ion homeostasis. Understanding the molecular mechanisms that affect salt tolerance and devising strategies to develop/breed salt-resilient crops have been the primary goals of plant salt stress signaling research over the past few decades. In this review, we reflect on recent major advances in our understanding of the cellular and physiological mechanisms underlying plant responses to salt stress, especially those involving temporally and spatially defined changes in signal perception, decoding, and transduction in specific organelles or cells.