Plants respond to high-salt environments by altering their osmotic potential. Over time, they have evolved a range of sensing and response mechanisms that regulate osmotic stress signals induced by salt stress (Christmann et al., 2013; Shabala et al., 2016; Gong et al., 2020; Wang et al., 2022b; Zhang et al., 2023a). Among these mechanisms, Ca²⁺ functions as a crucial secondary messenger in sensing and signaling under various abiotic stresses (Gong et al., 2020; Dong et al., 2022; Zhang et al., 2022a). In plants, the Reduced Hyperosmolality-Induced [Ca²⁺]_i Increase1 (OSCA1) gene encodes a hyperosmolarity-gated calcium channel that acts as an osmotic stress sensor. This channel detects rapid increases in cytosolic Ca²⁺ ([Ca²⁺]_cyt) levels triggered by osmotic stress (Knight et al., 1997; Yuan et al., 2014). In osca1 mutants, Ca²⁺ influx under high osmolarity is impaired, leading to reduced leaf transpiration and hindered root growth (Jojoa-Cruz et al., 2018; Liu et al., 2018; Maity et al., 2019). Similarly, in Arabidopsis thaliana, the MSCS-LIKE 8 (MSL8) gene encodes a membrane tension-gated ion channel that responds to osmotic stress by upregulating expression during low osmotic conditions. This process facilitates ion efflux, helping protect cells from hypoosmotic stress (Hamilton et al., 2015). These genes are central to osmotic stress sensing in plants.

Recent research has revealed that Ca²⁺-responsive proteins such as BONZAI (Chen et al., 2020a), plastid K⁺ exchange antiporters (Stephan et al., 2016), small-conductance mechanosensitive ion channel-like channels (Hamilton et al., 2015), and MID1-COMPLEMENTING ACTIVITY (MCA) channels (Kurusu et al., 2012a, b) activate downstream pathways in response to osmotic stress-induced changes in cell turgor pressure. Furthermore, SEUSS, a transcriptional co-regulator of AGAMOUS, plays a critical role in osmotic stress responses. Under hyperosmotic stress, SEUSS forms liquid-like nuclear condensates, which are associated with osmotic stress tolerance and gene expression regulation. The absence of SEUSS significantly impairs the expression of osmotic stress tolerance genes (Wang et al., 2022a).

Abscisic acid (ABA), a key plant hormone, regulates various physiological processes that allow plants to survive under adverse environmental conditions. The role of ABA in plant adaptation to drought, cold, and salinity stress is well established (Zhu, 2016). Salt-induced osmotic stress triggers the expression of ABA biosynthesis genes, including NINECIS-EPOXYCAROTENOID DIOXYGENASEs (NCEDs), ABA DEFICIENT (ABA), and ABA Aldehyde Oxidase (AAO3), promoting ABA accumulation and enhancing environmental adaptability (van Zelm et al., 2020; Du et al., 2023). Protein phosphorylation is key to ABA signal transduction under stress conditions. Conserved in A. thaliana, rice, and maize, clade A-type 2C protein phosphatases (PP2Cs) and subclass III SNF1-related protein kinase 2s (SnRK2s) are central to this process (Geiger et al., 2009; Sirichandra et al., 2009; Klingler et al., 2010; Sun et al., 2016; Min et al., 2019; Wu et al., 2019; Wang et al., 2020c). Salt-induced ABA accumulation is detected by the Pyrabactin Resistance 1/PYR1-Like/Regulatory Component of ABA Receptors (PYR/PYL/RCAR) family, which inhibits PP2Cs, leading to the release of SnRK2s. These SnRK2s phosphorylate downstream anion efflux channels and transcription factors, regulating stomatal closure and gene expression (Negi et al., 2008; Chen et al., 2020b; Takahashi et al., 2020). This phosphorylation activates ABA-responsive element (ABRE)/ABRE-binding factor transcription factors, which promote the expression of stress-responsive genes like β-AMYLASE1 and α-AMYLASE, contribute to osmolyte accumulation, and improve water and nutrient uptake (Thalmann et al., 2016).

ABA is synthesized in various plant tissues, including vascular tissues and guard cells, and is transported to long distances to ensure proper signal transduction (Christmann et al., 2005; Li et al., 2018). For instance, under dehydration stress, the CLAVATA3/Embryo-Surrounding Region-Related 25 (CLE25) peptide is induced in the roots and transported to the leaves via the vascular system, where it triggers ABA biosynthesis and accumulation, promoting stomatal closure (Takahashi et al., 2018). CLE25 loss-of-function mutants exhibit heightened sensitivity to salt stress (Takahashi et al., 2018).

In addition to PP2Cs and SnRK2s, mitogen-activated protein kinase (MAPK) cascades, composed of MAP kinase kinase kinases (MKKKs/MAP3Ks/MEKKs), MAP kinase kinases (MKKs/MAP2Ks/MEKs), and MAP kinases (MAPKs/MPKs), are pivotal in plant responses to osmotic stress (Gasulla et al., 2016). These MAPK cascades exhibit functional diversity, allowing plants to adapt to various environmental stimuli and internal demands (Zhang et al., 2022a). In Arabidopsis, the MKK4-MPK3 and MKKK20-MPK6 modules are vital in osmotic stress responses, and loss-of-function mutations in MKKs improve tolerance to dehydration and salinity (Kim et al., 2011, 2012). The bread wheat TMPK3 (wheat Mitogen-Activated Protein Kinase) plays a vital role in plant tolerance to salt and osmotic stresses. TMPK3 can autophosphorylate in vitro and is phosphorylated by the constitutively active Arabidopsis kinase AtMKK2. Additionally, TMPK3 phosphorylates its substrate, MAP kinase phosphatase 1. Notably, TMPK3 can compensate for the salt sensitivity in the Arabidopsis mpk3-1 loss-of-function mutant, and its overexpression significantly enhances plant tolerance to salt and osmotic stresses beyond the levels observed in wild-type plants (Ghorbel et al., 2023). Similarly, Raf-like protein kinases (RAFs), which act as MKKKs, are essential for ABA-triggered SnRK2 activation under salt-induced osmotic stress (Lin et al., 2021).

Accumulation of metabolic substances like proline, hydroxyproline, glycine betaine, sugars, and polyamines helps stabilize osmotic pressure changes under salt stress. These osmolytes mitigate water loss and improve cell turgor (Pommerrenig et al., 2007; Henry et al., 2015; Mansour and Ali, 2017). Salt-induced proline accumulation maintains H3K4me3 levels at the Δ1-PYRROLINE-5-CARBOXYLATE SYNTHETASE 1 locus (Feng et al., 2016). A metabolomics analysis of 266 maize inbred lines identified 37 metabolic biomarkers (METOs) associated with salt-induced osmotic stress (SIOS). Research further revealed that ZmCS3 (citrate synthase), ZmUGT (glucosyltransferase), and ZmCYP709B2 (cytochrome P450) contribute to METO-SIOS tolerance (Liang et al., 2021).

Multiple studies suggest that salt stress impacts plants through osmotic stress, to which they have developed various adaptive mechanisms. These include Ca²⁺ signaling, ABA pathways, protein phosphorylation, kinase cascades, and osmolyte accumulation.

Plants exposed to high-salt environments face two primary types of stress that are exposed to high-salt environments: osmotic stress, caused by changes in osmotic potential that reduce water absorption, and ionic toxicity, due to the accumulation of toxic ions such as Na⁺. While osmotic stress has been extensively reviewed, the study of Na⁺ transport and accumulation is equally critical for understanding salt stress in plants. As sessile organisms, plants rely primarily on their roots to absorb water, nutrients, and ions from their surroundings. In high-salt environments, Na⁺, the most abundant soluble cation, enters plants through various ion channels and transporters in the roots, including calcium-permeable non-selective cation channels (NSCCs) and high-affinity K⁺ transporters (HKTs) (Tester and Davenport, 2003; Mian et al., 2011) ( Figure 2 ).

Transpiration leads to significant water loss, which in turn increases the concentration of ions like Na⁺ within plant tissues. To combat this, plants have developed sophisticated mechanisms to exclude excess salts from their cells (Munns et al., 2020). Studies have shown that plants primarily rely on membrane transporters responsible for Na⁺ uptake, export, and compartmentalization to limit Na⁺ accumulation, thereby mitigating salt stress. These mechanisms are vital for maintaining intracellular ion homeostasis and preserving normal physiological functions in salt-stressed plants (Gong et al., 2020; Liang et al., 2024). In recent years, an increasing number of studies have reported that membrane transporters and membrane proteins play a crucial role in the salt tolerance of plants (Isayenkov and Maathuis, 2019; Banik and Dutta, 2023; Dutta, 2023; Mishra et al., 2024). While these processes have been extensively studied in A. thaliana, they have also been observed in a variety of crop species, highlighting their broader relevance.

Roots serve as the primary organs for Na⁺ absorption in plants. The ion traverses the root epidermis, cortex, and endodermis before entering the xylem, where it is transported to the stem tissue. Excessive accumulation of Na⁺ in the stem can lead to toxic effects, prompting plants to evolve various mechanisms to limit Na⁺ entry into the root xylem and facilitate its recovery, thereby reducing transport to the stem.

HKT-type transporter proteins play a pivotal role in the retrieval of Na⁺ from the root xylem, significantly contributing to plant salt tolerance (Gong et al., 2020). Members of the HKT1 subfamily are known to reclaim Na⁺ from the root xylem, thereby minimizing its transport from roots to stems. This includes AtHKT1 in Arabidopsis; OsHKT1;1, OsHKT1;4, and OsHKT1;5 in rice; TaHKT1;4 and TaHKT1;5 in wheat; and ZmHKT1;1 and ZmHKT1;2 in maize (Ren et al., 2005; Huang et al., 2006; Munns et al., 2012; Byrt et al., 2014; Campbell et al., 2017; Oda et al., 2018; Zhang et al., 2018, 2023b; Wang et al., 2024c). In Arabidopsis, the athkt1 mutants exhibit excessive Na⁺ accumulation and hypersensitivity to Na⁺ in the stem (Berthomieu et al., 2003). AtHKT1 functions in root parenchyma cells to retrieve Na⁺ from the root xylem, thereby mitigating Na⁺ accumulation in the stem. Specifically, overexpression of AtHKT1 in the root stele enhances salt tolerance in Arabidopsis (Moller et al., 2009). Under salt stress, PP2C49, a type G PP2C, inhibits Na⁺ permeability of AtHKT1 (Chu et al., 2021).

In rice, OsHKT1;5 is crucial for removing Na⁺ from the root xylem, thus conferring salt tolerance to the plant (Ren et al., 2005; Kobayashi et al., 2017). Salt stress enhances the interaction between OsDNAJ15 and OsBAG4 in the nucleus, promoting the formation of transcriptional complexes that activate OsHKT1;5 (Liu et al., 2023). Additionally, the loss of function of OsWRKY53 facilitates Na⁺ homeostasis mediated by OsMKK10.2 and OsHKT1;5 (Yu J. et al., 2023). Literature also suggests that epigenetic modifications are involved in gene expression mediated by AtHKT1 and OsHKT1;5 under salt stress (Baek et al., 2011; Wang et al., 2020a; Liu et al., 2022a, b). Mutations in OsHKT1;1 can affect Na⁺ accumulation in rice roots and alter salt tolerance (Campbell et al., 2017).

In wheat, TaHKT1;4 and TaHKT1;5 are major genes that reduce Na⁺ transport and accumulation, enhancing salt tolerance. TaHKT1;4 sequesters Na⁺ in the leaf sheath, minimizing its transport and accumulation in leaf blades (Huang et al., 2006; James et al., 2006). Conversely, TaHKT1;5 functions similarly to AtHKT1, facilitating the retrieval of Na⁺ from the root xylem (Byrt et al., 2007). The SPL6-HKT1;5 module offers a target for the molecular breeding of salt-tolerant crops (Wang et al., 2024c). Notably, TaHKT1;5 enables durum wheat to increase grain yield by 25% in saline soils, significantly enhancing its economic value for developing salt-tolerant, high-yielding crop varieties (Munns et al., 2012).

In maize, the functions of ZmHKT1;1 and ZmHKT1;2 are closely linked to salt tolerance. Mutations in ZmHKT1;1 result in increased Na⁺ content in the leaves and a salt-sensitive phenotype (Zhang et al., 2018). ZmHKT1;2 is also associated with Na⁺ content in the shoots of maize seedlings under salt stress (Zhang et al., 2019, 2023b). Modern research indicates that salt tolerance in maize is a complex trait governed by multiple genes that influence Na⁺ transport and distribution within the plant.

The HKT1 subfamily of transporters primarily mediates sodium ion transport. In contrast, the HKT2 subfamily, exclusive to monocotyledonous plants, uniquely transports both sodium and potassium ions (Hamamoto et al., 2015; Ali et al., 2019). However, HKT2 transporters can also mediate Na⁺ uptake. For instance, ZmNC2/ZmHAK4 functions as a Na⁺-selective transporter located in the xylem parenchyma cells of the root stele, reducing Na⁺ accumulation in the stem by facilitating Na⁺ removal from the root xylem (Zhang et al., 2019). In rice, OsHKT2;1, localized to the plasma membrane, mediates Na⁺ uptake but is inhibited under salt stress (Horie et al., 2007). OsHAK12 promotes Na⁺ exclusion from stem tissues via a mechanism akin to ZmHAK4 ( Figure 2 ) (Zhang et al., 2021).

Salt stress also promotes the development of the Casparian strip (CS), which forms a barrier that prevents salt ions from entering the root stele through the apoplastic pathway (Chen et al., 2011; Wang et al., 2022c). In summary, by minimizing the transport of Na⁺ from roots to shoots and enhancing its retrieval from the root xylem, plants can effectively mitigate the toxic effects of salt stress.

The discovery of SOS genes has provided a foundational understanding of plant salt tolerance. Over the past few decades, scientists have increasingly recognized the central role of the SOS signaling pathway in mediating Na⁺ extrusion from plant roots (Shi et al., 2002; Yang and Guo, 2018b). Through mutant screening experiments, researchers have identified various salt-sensitive mutants (sos mutants), cloned SOS genes, and thoroughly characterized their functions. It is now widely accepted that the SOS signaling pathway comprises three key proteins: SOS1, SOS2, and SOS3 (Zhu, 2001).

The SOS1 gene is highly conserved across sequenced genomes and encodes a plasma membrane Na⁺/H⁺ antiporter that utilizes the H⁺ gradient to drive Na⁺ extrusion, thereby lowering cytoplasmic Na⁺ concentrations ( Figure 2 ) (Shi et al., 2000, 2002, 2003; Steinhorst et al., 2022; Zhang et al., 2023c, d). In A. thaliana, SOS1 uniquely possesses a long cytoplasmic C-terminal region exceeding 700 amino acid residues (Shi et al., 2000). This C-terminal region contains a self-inhibitory domain that interacts with upstream sequences harboring putative cyclic nucleotide monophosphate (cNMP) binding motifs, inhibiting SOS1 transport activity under normal conditions. These motifs are essential for SOS1 function, and mutations in these motifs lead to its inactivation (Shi et al., 2000). This suggests that SOS1 may be regulated by cyclic nucleotides, signaling molecules that mediate plant environmental adaptation and play roles in responses to salt and osmotic stress (Shabala et al., 2015; Swiezawska et al., 2018). The C-terminal region also interacts with numerous regulatory proteins and undergoes phosphorylation, modulating SOS1 antiporter activity (Fliegel, 2019). Under high-salt conditions, serine residues within this self-inhibitory domain are phosphorylated by SOS2, activating SOS1 to transport Na⁺ out of the cell and prevent salt toxicity (Quintero et al., 2011). The SOS2 gene encodes a member of the SNF1-related kinase 3 (SnRK3s), also known as CBL-interacting protein kinase 24 (CIPK24), which comprises 25 members in A. thaliana. Under high-salt conditions, the autoinhibition of SOS2 is relieved, enabling it to activate SOS1 through phosphorylation (Liu et al., 2000; Guo et al., 2001; Quintero et al., 2002). Meanwhile, SOS3 (also known as CBL4) encodes a Ca²⁺-binding protein with three EF-hand motifs that senses the elevation of Ca²⁺ levels triggered by salt stress. Its family includes 10 members (Liu and Zhu, 1998; Ishitani et al., 2000; Kim et al., 2007; Quan et al., 2007; Steinhorst et al., 2022; Yang and Guo, 2018a; Zhu, 2016).

The SOS3–SOS2–SOS1 module plays a critical role in plant salt tolerance. Mutants lacking any of these three genes exhibit heightened sensitivity to NaCl, underscoring their essential function in conferring salt tolerance. In this signaling pathway, SOS3 detects the salt-induced rise in Ca²⁺ levels and binds to the autoinhibitory domain of SOS2, activating it. The N-terminus of SOS3 is myristoylated, allowing it to bind to the plasma membrane and recruit the SOS3–SOS2 complex, where SOS2 phosphorylates SOS1. This phosphorylation enhances the Na⁺/H⁺ antiporter activity of SOS1, promoting Na⁺ extrusion and lowering intracellular Na⁺ concentrations. The Na⁺ extrusion mediated by the SOS3–SOS2–SOS1 module is a critical mechanism for maintaining ion homeostasis and preventing salt toxicity under high-salt conditions (Halfter et al., 2000; Qiu et al., 2002; Kim et al., 2007; Quan et al., 2007; Quintero et al., 2011; Steinhorst et al., 2022; Zhang et al., 2023c, d).

The CBL–CIPK signaling pathway plays a pivotal role in plant responses to various abiotic stresses (Weinl and Kudla, 2009; Kudla et al., 2018). Under salt stress, SOS2 specifically interacts with and phosphorylates SCaBP8 (also known as CBL10), promoting the recruitment of SOS2 to the plasma membrane, where SOS2 then phosphorylates SOS1, enhancing its Na⁺ extrusion transporter activity (Quan et al., 2007; Lin et al., 2009). Additionally, the SOS2–SCaBP8 complex phosphorylates and inhibits the putative Ca²⁺-permeable transporter AtANN4, forming a negative feedback loop to fine-tune Ca²⁺ signaling in response to salt stress (Ma et al., 2019). Research indicates that the SOS2–SOS3 complex primarily functions in the roots, while the SOS2–SCaBP8 complex acts predominantly in the shoots. These complexes confer salt tolerance by enhancing SOS1 transport activity (Quan et al., 2007; Lin et al., 2009; Yang and Guo, 2018a). Furthermore, the cbl8 mutant exhibits hypersensitivity to severe salt stress, highlighting the importance of CBL8 in salt stress responses (Steinhorst et al., 2022). CBL5, an ortholog of CBL4 and CBL10 in Arabidopsis, interacts with and recruits CIPK8 and CIPK24 to the plasma membrane. This interaction is essential during seed germination, where CBL5 helps protect seeds and germinating seedlings from salt stress via the CBL5-CIPK8/CIPK24-SOS1 pathway (Xie et al., 2024). Another member of the CIPK family, CIPK8, forms a complex with SCaBP8/CBL10 and SOS1, promoting salt tolerance (Yin et al., 2020).

Numerous regulatory factors fine-tune the SOS signaling pathway, enhancing plant responses to salt stress (Ali et al., 2023). In parallel with the regulation at the post-translational level, several protein complexes have been identified recently that regulate the SOS pathway core components transcriptionally. Among them, the histone linker protein HIS1-3 (negatively) and the transcription factor WRKY1 (positively) are two proteins that regulate all three core elements of the SOS pathway. HIS1-3 and WRKY1 bind to the same loci on the chromatin of the SOS pathway genes and regulate their transcription (Wu et al., 2022). Short Root in Salt Medium1(RSA1)-RSA1 Interacting Transcription Factor1(RITF1) is another complex that positively regulates the SOS1 transcript through a nuclear calcium signaling pathway (Shi et al., 2003; Guan et al., 2013). MPK4-MYB42 is a module that activates SOS2 transcription in a UBC1/UBC2-dependent manner (Sun Y. et al., 2020; Zarreen et al., 2022). The transcription factor plant AT-rich sequence and zinc-binding protein 2 (PLATZ2) suppresses SOS3/SCaBP8 transcription, thereby negatively regulating salt stress tolerance (Liu S. et al., 2020). Under normal conditions, ABI2 (Ohta et al., 2003), GIGANTEA (GI) (Kim et al., 2013), 14-3-3 proteins, and SOS2-like protein kinase 5 (PKS5) (Zhou et al., 2014; Yang et al., 2019c) interact with SOS2 to inhibit its kinase activity. The interaction between SOS2 and ABI2 suggests a potential link between the salt stress response and ABA signaling pathways. Under high-salt conditions, GI is degraded, releasing its inhibition of SOS2, which subsequently activates SOS2 to promote salt tolerance (Kim et al., 2013). PKS5-mediated phosphorylation of SOS2 enhances its interaction with 14-3-3 proteins, but during salt stress, elevated Ca²⁺ levels promote 14-3-3 binding to PKS5, inhibiting PKS5 kinase activity and weakening the interaction between 14-3-3 and SOS2, thereby activating SOS2 (Yang et al., 2019c). GRIK1 phosphorylates and promotes SOS2 activity (Barajas-Lopez et al., 2018), while VPS23A enhances the SOS2–SOS3 interaction, promoting SOS2 localization to the plasma membrane (PM) (Lou et al., 2020). The SOS signaling pathway has been shown to connect salt stress with plant hormone signaling pathways (Yu et al., 2020). SOS2 enhances salt tolerance by inhibiting the kinase activity of CONSTITUTIVE TRIPLE RESPONSE1 (CTR1) through phosphorylation at serine 87 (S87), thereby activating the ethylene signaling response (Li et al., 2024). In addition, AFP2, a plant-specific ABI5-binding protein, serves as a negative regulator in the ABA signaling pathway and plays a key role in salt tolerance during seed germination. AFP2 mutations increase sensitivity to salt stress. SOS2 physically interacts with and stabilizes AFP2, promoting the degradation of ABI5, a transcription factor that negatively regulates seed germination under salt stress. These findings suggest a potential link between salt stress and the ABA signaling pathway, opening new possibilities for enhancing plant resilience to environmental challenges (Wang et al., 2024a). Under salt stress, SCaBP8 inhibits the activity and PM localization of two type-D protein phosphatases (PP2C D6/D7), thereby activating SOS1 (Fu et al., 2023). PAMP-induced secreted peptide 3 (PIP3) binds and activates receptor-like kinase 7 (RLK7), which in turn activates MPK3 and MPK6, enhancing SOS1 activity and promoting Na⁺ homeostasis via ethylene/ROS signaling (Yu et al., 2010; Li et al., 2014; Zhou et al., 2022a). Salt-induced cytosolic Ca²⁺ increases facilitate the activation of phospholipase D (PLD) at the PM, generating the lipid messenger phosphatidic acid (PA) (Wang et al., 2006; Do et al., 2019). PA accumulation promotes the localization and enhances the kinase activity of SOS2 and MPK6 at the PM, facilitating SOS1-mediated Na⁺ efflux (Yu et al., 2010; Li et al., 2023a).

Beyond Arabidopsis, the SOS pathway is conserved in rice (Martinez-Atienza et al., 2007; El Mahi et al., 2019), maize (Zhang et al., 2016a; Zhou et al., 2022b; Li et al., 2023a, b), wheat (Feki et al., 2011; Yang et al., 2024), soybean (Zhang et al., 2022b), and tomato (Wang et al., 2021; Hong et al., 2023). In summary, the SOS pathway and its regulatory factors play crucial roles in promoting Na⁺ efflux from the roots into the soil solution and enhancing salt tolerance in shoot tissues (Quan et al., 2007; Liang et al., 2024).

Researchers have long recognized that Na⁺ compartmentalization serves as an effective mechanism for plants to mitigate Na⁺ toxicity under salt stress conditions. Excess Na⁺ absorbed by plant roots can be sequestered into vacuoles or transported to the aerial parts of the plant. The central vacuole is particularly well-suited for Na⁺ sequestration, as it reduces cytoplasmic Na⁺ accumulation. This sequestration offers several advantages: it decreases Na⁺ concentration in the cytoplasm, preventing transport from underground parts to aerial tissues, thereby protecting plants from salt-induced toxicity. Furthermore, Na⁺ accumulation in vacuoles can act as an osmoregulatory substance, reducing cell water potential and promoting water uptake under salt stress (Yang and Guo, 2018a). While the size of plant cells is finite, the process of sequestering Na⁺ into vacuoles is an effective cellular strategy throughout the plant’s life cycle, safeguarding against Na⁺ toxicity caused by salt stress.

The sequestration of Na⁺ in vacuoles is mediated by vacuolar Na⁺/H⁺ exchangers (NHXs), which rely on the H⁺ gradient established by vacuolar H⁺-ATPases (V-ATPase, VHA) and H⁺-pyrophosphatases (V-PPase, VP) (Drozdowicz and Rea, 2001; Brini and Masmoudi, 2012). The NHX gene family is conserved across various plant species, including Arabidopsis, tomato, and several crops (Apse et al., 1999; Zhang and Blumwald, 2001; Zhang et al., 2001; Zhang and Shi, 2013). In Arabidopsis, the NHX family comprises six members, and overexpression of the AtNHX1 gene has been shown to enhance salt tolerance in multiple plant species (Zhang and Shi, 2013). Studies indicate that the C-terminal region of AtNHX1 interacts with calmodulin (CaM) within the vacuole, inhibiting the transport activity of AtNHX1 in a Ca²⁺-dependent manner (Yamaguchi et al., 2003, 2005). Gain-of-function mutations in AtNHX1 can suppress salt hypersensitivity in sos1 mutants by limiting Na⁺ accumulation in the cytoplasm and its transport to the shoots (Pabuayon et al., 2021). Additionally, AtNHX1 and AtNHX2 are instrumental in K⁺ accumulation in vacuoles and the regulation of vacuolar pH (Bassil et al., 2011b; Barragan et al., 2012). AtNHX5 and AtNHX6, localized in the Golgi, trans-Golgi vesicles, and prevacuolar compartments, are critical for maintaining the pH of these compartments (Bassil et al., 2011a; Reguera et al., 2015). The nhx5 nhx6 double mutants exhibit salt hypersensitivity, likely due to the mislocalization of vacuolar transporters essential for Na⁺ sequestration (Bassil et al., 2011b).

In addition to NHX proteins, the vacuolar membrane-localized SCaBP8 also plays a pivotal role in Na⁺ sequestration by interacting with SOS2 (Kim et al., 2007; Yang et al., 2019b). Moreover, salt-induced endocytosis contributes to Na⁺ accumulation in vacuoles. For example, overexpression of AtRab7, a gene involved in vesicle trafficking regulation, enhances endocytosis in protoplasts, roots, and leaves, promoting Na⁺ accumulation in vacuoles (Mazel et al., 2004; Hamaji et al., 2009; Golani et al., 2013). In summary, NHX-type Na⁺/H⁺ antiporters are essential for mediating Na⁺ sequestration in plant cells, thereby promoting salt tolerance, growth, and development ( Figure 2 ) (Zhang and Shi, 2013). However, the membrane transport mechanisms involved in intracellular Na⁺ sequestration remain poorly understood and warrant further investigation (Liang et al., 2024).

In addition to Na⁺, maintaining K⁺ homeostasis under high salinity conditions is equally crucial for plant growth and development. Achieving K⁺ homeostasis in saline environments necessitates facilitating K⁺ influx while inhibiting K⁺ efflux (Yang and Guo, 2018a, b). K⁺ influx primarily relies on transporters such as HAKs and AKT (Gierth et al., 2005). In Arabidopsis, the HAK5 protein promotes high-affinity K⁺ uptake induced by K⁺ deprivation (Ragel et al., 2015). Similarly, in rice, OsHAK1, OsHAK5, OsHAK16, and OsHAK21 function analogously to Arabidopsis HAK5, enhancing K⁺ uptake under salt stress (Song et al., 2021). The AKT1 transporter is responsible for primary K⁺ uptake in Arabidopsis roots (Lagarde et al., 1996). Under salt stress, SOS2 promotes the phosphorylation of SCaBP8, alleviating its inhibitory effect on AKT1 and enhancing K⁺ uptake in the roots (Li et al., 2023). Conversely, the ZmHKT2 protein in maize negatively regulates K⁺ accumulation in the stems, which reduces the salt tolerance of maize (Cao et al., 2019). TaHKT9-B is a K⁺-preferring HKT transporter. The tae-miR390/TaTAS3/TaARF4/TaHKT9-B module has been identified as a crucial regulatory pathway in wheat under salt stress, offering valuable genetic resources for breeders aiming to enhance wheat salt tolerance (Du et al., 2024). These findings underscore the significance of maintaining K⁺ homeostasis for plant salt tolerance, emphasizing the need to study K⁺ transport mechanisms to improve crop salt tolerance.

Excessive Cl⁻ accumulation under salt stress can limit NO₃ ⁻ uptake, transport, and assimilation (Li et al., 2017), potentially leading to Cl⁻ toxicity (Ren et al., 2021). Consequently, Cl⁻ uptake and transport processes are intricately linked to plant salt tolerance. Reported transporters include the Arabidopsis nitrate transporter/peptide transporters (AtNPF2.4 and AtNPF2.5), slow-type anion channel associated 1 homologs (AtSLAH1 and AtSLAH3), cation/Cl⁻ cotransporters (AtCLCc and AtCLCg), aluminum-activated malate transporter 9 (ALMT9), and the rice MATE (multidrug and toxic compound extrusion family) transporter BIG RICE GRAIN 1 (BIRG1). Additionally, ZmMATE29, type-A response regulator (ZmRR1), and histidine phosphotransfer protein 2 (ZmHP2) in maize maintain Cl⁻ homeostasis by facilitating Cl⁻ retrieval from the root xylem, vacuolar Cl⁻ accumulation, or Cl⁻ efflux from the roots, thereby regulating plant salt tolerance ( Figure 2 ) (Colmenero-Flores et al., 2007; Negi et al., 2008; Jossier et al., 2010; Teakle and Tyerman, 2010; De Angeli et al., 2013; Baetz et al., 2016; Cubero-Font et al., 2016; Li et al., 2016a, b; Henderson et al., 2018; Ren et al., 2021; Yin et al., 2023).