In terrestrial vascular plants, the cell wall is primarily composed of cellulose, a homopolymer made up of repeating glucose subunits linked by β (1-4) bonds (Ellinger and Voigt, 2014; Schneider et al., 2016). Cellulose plays a crucial role as the main load-bearing component of the cell wall, providing mechanical support. The synthesis of cellulose is an active process, with its synthesis trajectory guided by microtubules within the plant cell. During this process, a heterotrimeric rosette structure known as CesA interacts with Plant Oligosaccharide Binding Protein 2/Cellulose Synthase Interacting Protein 1 (POM2/CSI1) to facilitate cellulose production (Bringmann et al., 2012). The role of CesA in cellulose synthesis has been explored in previous studies (Joshi and Mansfield, 2007; Lampugnani et al., 2018). A mutation in the catalytic domain of CESA6 results in reduced cellulose content in plants (Huang et al., 2023). Although there is still a lack of extensive experimental evidence showing how CesA genes function under salt stress conditions in plants (Heyndrickx and Vandepoele, 2012). General Control Non-repressed Protein 5 (GCN5) plays a key role in regulating cellulose synthesis in salt-sensitive Arabidopsis thaliana by modulating the transcription of cellulose biosynthetic genes, thereby contributing to enhanced salt stress tolerance (Zheng et al., 2019). Mutants deficient in cellulose, such as cesa6, pom2/csi1, and the Companion of Cellulose Synthases (CC) mutant, display heightened sensitivity to salt stress. These mutants display a sensitive phenotype to salt stress. This increased sensitivity is primarily due to impaired cellulose biosynthesis, which compromises cell wall integrity and reduces the plant’s ability to cope with environmental stressors (Endler et al., 2015; Zhang et al., 2016a).

Salt stress inhibits cellulose synthesis, leading to altered cell wall structure and impaired plant growth ( Table 2 ). This inhibition is partly due to the depolymerization of cortical microtubules (MTs), which disrupts the delivery and orientation of the cellulose synthase complex (CSC)—a plasma membrane-localized, multi-subunit protein complex responsible for polymerizing UDP-glucose into β-1,4-glucan chains that form cellulose microfibrils (Wang et al., 2007). The coordination between CSC and MTs is facilitated by the CC proteins, which act as molecular bridges by simultaneously binding to CSC and MTs, thereby aligning cellulose deposition with cytoskeletal dynamics. However, the precise feedback mechanism by which MTs rely on CSC—and ultimately the cell wall—for stress signal perception remains unresolved.

Moreover, proper cellulose biosynthesis under salinity is regulated by protein glycosylation. The N-glycosylation pathway in the endoplasmic reticulum (ER) modulates salt tolerance and CSC functionality in a mature N-glycan-dependent manner. In particular, complex N-glycans are essential for the activity of KORRIGAN 1 (KOR1, also known as RADIALLY SWOLLEN2 or RSW2), a membrane-bound endo-1,4-β-glucanase that contributes to cellulose microfibril elongation (Kang et al., 2008). Additionally, transcriptomic analyses in the salt-tolerant Dendrobium officinale revealed that CELLULOSE SYNTHASE-LIKE A (CSLA) genes are upregulated under salt stress and are involved in the biosynthesis of mannan-type hemicelluloses, highlighting the broader impact of salt stress on non-cellulosic polysaccharide production (He et al., 2015).

Hemicellulose composition in the cell wall varies between species but is mainly composed of a polysaccharide backbone linked by β (1→4) linkages. Glucans with β (1→3, 1→4) links are grouped with xyloglucans, xylans, glucomannans, mannans, and other similar families (Scheller and Ulvskov, 2010). In dicotyledonous plants, xyloglucans (XyGs) typically constitute 20–25% of the primary cell wall and serve as the major hemicellulose component. In contrast, monocots possess type II primary walls in which glucuronoarabinoxylan dominate, and XyGs account for only 1–5% of total wall polysaccharides (Gigli-Bisceglia et al., 2020; Alvarez et al., 2024).

In dicots, XyGs form tightly bound complexes with cellulose, creating “hotspots” that play a central role in regulating wall mechanics. These hotspots bear localized mechanical stress during cell expansion and wall loosening, while pectins assist by modulating wall porosity and promoting cell elongation and division (Cosgrove and Jarvis, 2012). However, despite the structural significance of XyG-cellulose interactions, the precise biochemical impact of these hotspots on the mechanical properties of the cell wall remains incompletely understood and requires further investigation.

XyGs consists of a β-(1,4)-linked glucose backbone with α-(1,6)-linked xylosyl side chains. In some cases, these side chains are further modified with fucose or galactose, resulting in a complex, branched structure (Schultink et al., 2014; Pauly and Keegstra, 2016). The XyGs are a spacer polymer in the primary cell wall (Thompson, 2005; Anderson et al., 2010). Xylan is widely known as β-(1-4)-linked xylose residue decorated by glucuronic acid to form glucuroxylan. Xylan is mainly accumulated in the secondary cell wall; similarly, it is also present in some algae and monocots. The biosynthesis of XyGs takes place in the Golgi apparatus via glycan synthase and glycosyltransferases. XyGs are then exported to the plasma membrane through packing in vesicles and released into the extracellular matrix, where modification takes place via multiple extracellular enzymes, and eventually become part of the cell wall (Pauly and Keegstra, 2016).

Many studies have been conducted to better understand how hemicellulose, specifically xyloglucan, functions under salt stress ( Table 3 ). Under salinity stress, xyloglucan is a metabolic inducer that triggers different physiological responses (Páez-Watson et al., 2020). The xyloglucan endotransglucosylase/hydrolase (XTH) enzyme plays a key role in altering cell wall morphology by cleaving and restructuring XyGs, thereby facilitating the reorganization of the cell wall matrix. The reduced end of XyG is then linked to the non-reducing end of another XyG polymer or oligomer. The gene CaXTH3 is involved in cell wall remodeling by accumulating starch content, which enables the plant mesophyll cell to retain humidity, and is actively involved in numerous cellular processes and salinity stress tolerance in transgenic Arabidopsis seedlings (Cho et al., 2006; González-Pérez et al., 2018). Additionally, the involvement of XTH19 and XTH23 in the brassinosteroid (BR) signaling elucidates how the BES1-dependent pathway affects lateral root development under salinity stress (Xu et al., 2020). Furthermore, XTH30 negatively regulates salt tolerance by promoting microtubule depolymerization and reducing crystalline cellulose deposition (Yan et al., 2019). Additionally, under salinity stress, the hemicellulose in the cell wall of Artemisia annua shows an increase in xylose content (Correa-Ferreira et al., 2019). The xyloglucan plays a significantly important role in defining the cell shape by regulating the cellulose microfibril’s loosening and tightening events during cell growth and maturation. However, little is known about how salt stress impacts the XyG structure and thus plant growth and development.

Pectin is a major component of the primary cell wall and the most diverse polysaccharide. Backbone of pectin consists of α-(1,4)-linked galacturonic acid (GalA), that are classified into three types: complex branched rhamnogalacturonan II (RG II), homogalacturonan (unbranched HG), and rhamnose-alternated (RG I), i.e., rhamnogalacturonan I α-(1,4) GalA and α-(1,2) rhamnose (Atmodjo et al., 2013; Amos et al., 2018). The pectin structure is strengthened by Ca²⁺-bridged HG and dimerized RG-II, which is also linked to boron ions (B³⁺). These interactions contribute to the strength of the primary cell wall in terrestrial plants (Liu et al., 2012; Oda and Fukuda, 2012; Kim et al., 2020). Pectin interacts with cellulose at RG-I blocks (arabinan galactan side chains) (Zykwinska et al., 2005). RG-II bonding is reinforced by the Ca²⁺ pectate bond. HG biosynthesis is mediated by galacturonosyl transferases (GAUTs). A detailed review of pectin biosynthesis and structure has been published by Zhang et al. (2021).

Pectin in the cell wall plays a vital role during cell proliferation and plant growth by providing flexibility (Peaucelle et al., 2012). FERONIA (FER) receptor kinases localized at the plasma membrane act as a sensor to sense pectin-associated cell wall damage during salinity stress (Feng et al., 2018; Verger and Hamant, 2018). Pectin methylesterase inhibitor (PMEI) negatively regulates salt resistance and reduces primary root growth (Jithesh et al., 2012). PMEIs maintain a high degree of pectin methyl esterification by inhibiting the activity of pectin methylesterases (PMEs). This suppression of PME activity limits the formation of calcium-mediated cross-links between homogalacturonan chains, thereby preserving cell wall plasticity. Such regulation is vital for maintaining primary root growth under saline conditions, as increased pectin methyl esterification enhances cell wall loosening and facilitates cell elongation and expansion (Peaucelle et al., 2011). The dynamic modulation of pectin structure through the PME–PMEI balance demonstrates a critical mechanism by which plants sustain root architecture and cellular integrity under abiotic stress.

Under salinity stress, the disruption of pectin structure plays a crucial role in root growth regulation (Chen et al., 2018). In developing plant cells, invasive Na⁺ competes with Ca²⁺ for binding sites on galacturonic acid residues in homogalacturonan, destabilizing the Ca²⁺-crosslinked structure. Similarly, the borate-crosslinked structure of GCN5 is also disrupted, weakening the integrity of the cell wall (Munarin et al., 2012). This structural compromise is sensed by FER, a cell wall integrity (CWI) sensor protein, which activates signaling pathways to mitigate the damage and restore growth (Feng et al., 2018). PMEIs, including salt tolerant Chorispora bungeana CbPMEI1, regulate PME activity, preventing excessive pectin demethylesterification that could otherwise increase the vulnerability of pectin to degradation under salt stress. Levels of pectin in the cell wall are modified by TRICHOME SPECIFIC DEFECTIVE 2 (TSD2) in rice, when exposed to salinity stress (Fang et al., 2019). Pectin methylesterase 31 (PME31), localized at the plasma membrane, positively modulates salt stress tolerance in Arabidopsis by decreasing RD29A, DREB2A, and RD29B expression, thereby reducing stress-induced ABA signaling and osmotic stress responses, ultimately contributing to cell wall stability and adaptive growth under saline conditions (Yan et al., 2018). Pectin plays a key role in regulating cell growth, and under salt stress, cellulose content increases while pectin levels decrease ( Table 4 ). These findings suggest that salt stress enhances the rigidity of the cell wall, which inhibits root growth (An et al., 2014).

The secondary cell wall in plants mainly consists of cellulose, hemicellulose (primarily xylans and glucomannans), and lignin, along with various structural proteins and enzymes. Lignin is hydrophobic in nature, forms a substantial part of secondary cell wall biomass, and contributes to the rigidity of the plant (Scheller and Ulvskov, 2010). Both the quantity and composition of lignin varies across plant species. Lignin is structurally a complex polyphenolic polymer that integrates into cellulose and hemicellulose networks, providing mechanical strength, hydrophobicity, and rigidity to the secondary cell wall. It is primarily composed of three monolignols, i.e., coniferyl alcohol, ρ-coumaryl alcohol, and sinapyl alcohol, which are represented as guaiacyl (G), ρ-hydroxyphenyl (H), and syringyl (S), respectively, in the lignin polymer (Bonawitz and Chapple, 2010). The composition of these monolignols differs between species and cell types. The biosynthesis and acylation of lignin (monolignols) have been briefly described (Vanholme et al., 2019). Salt stress alters lignin concentration ( Table 5 ). In response to salinity stress, maize cell walls decrease polysaccharides and arabinosyl feruloylation in arabinoxylan while increasing S-unit lignin polymers (Oliveira et al., 2020). Genotype-specific modifications in cell wall composition, including lignin and polysaccharide dynamics, play a critical role in determining plant tolerance to salt and drought stress by influencing wall plasticity and stress adaptability (Calderone et al., 2024). Salt stress increases lignin deposition in the root tracheary elements. A model was proposed in which increased lignin deposition limits ion uptake, enhances selective water transport through the symplastic pathway, reduces apoplast water flow, and restricts root growth (Sanchez-Aguayo et al., 2004). The change in lignin content and composition in response to abiotic and biotic stress has been briefly discussed by Moura et al. (2010), and recent studies suggest that selective downregulation of lignin can further improve salt stress tolerance by enhancing cell wall flexibility and facilitating better ion homeostasis in plants (Dokka et al., 2024).

Recent studies have highlighted the genetic and molecular regulation of lignin biosynthesis and its critical involvement in enhancing salt stress tolerance through diverse signaling and transcriptional networks. Mutation of histone acetyltransferase GCN5 suppresses the expression of chitinase like gene 1 (CTL1), which is essential for cellulose and lignin synthesis and salt tolerance in Arabidopsis (Zheng et al., 2019). The overexpression of Superoxide Dismutase (SOD), and Ascorbate Peroxidase (APX) in Solanum tuberosum L. induces cell wall lignification and promotes expression of different associated transcription factors during salt stress (Shafi et al., 2017). In apple, MYB46 enhances salt stress tolerance by increasing lignin accumulation and secondary cell wall synthesis and activates ABA-dependent and independent pathways that ultimately trigger various other defense responses (Chen et al., 2019). Overexpression of the sweet potato SWPA4 gene in transgenic tobacco increases lignin deposition, hydrogen peroxide (H₂O₂) levels, and transcription of apoplast-related genes, which promote salt tolerance. Similarly, the two cultivars of soya bean with contrasting salt tolerance showed increased cell wall cellulose, pectin, and uronic acid under salt stress (An et al., 2014). Non-methylated uronic acid in the leaf cell wall contributes to salt resistance by reducing Na⁺ accumulation in plant tissues (Uddin et al., 2014). The dynamic regulation of lignin content and composition under salt stress reinforces cell wall integrity, modulates water and ion transport, and enhances stress resilience, highlighting its crucial role in plant adaptation to saline environments. These structural variations shape their remodeling responses, including differences in pectin de-esterification, lignification, and reactive oxygen species (ROS) signaling (Haas and Peaucelle, 2021).

The plant cell wall is not only vital for structural integrity but also for transducing environmental signals. Mechanical measurements using atomic force microscopy and Fourier-transform infrared analysis revealed that the cell wall structure is mechanically homogeneous; nevertheless, during the growth phase, stiffness increases on average as heterogeneity grows (Radotic et al., 2012). The assembly and regulation of cell wall proteins are essential for plant function, particularly in response to salt stress ( Table 6 ). The heterotrimeric Gβ subunit AGB1 interacts with the receptor-like kinase FER and the peptide ligand RALF1 to modulate salt stress responses, highlighting a key signaling module in cell wall-associated salinity sensing (Yu and Assmann, 2018). LRXs further contribute to signaling pathways, interacting with RALF peptides, and coordinating growth regulation under stress conditions (Zhao et al., 2018; Wang and Gou, 2020). Structural proteins such as extensins play a vital role in maintaining cell wall architecture (Lamport et al., 2011). STELLO (STL) proteins in the Golgi facilitate CSC formation and may play a role in glycosylation, although their specific substrates are unknown (Zhang et al., 2016b). The CSC protein secreted from the endomembrane to the plasma membrane is altered depending on different aspects, such as the actin cytoskeleton via polymerization and depolymerization (Zhang et al., 2019), the pH of the endomembrane system (Luo et al., 2015), and interaction with proteins such as SHOU4 and TRANVIA (Polko et al., 2018; Vellosillo et al., 2021). Cortical microtubules coordinate the delivery of CSC to the plasma membrane (Gutierrez et al., 2009). Plants tolerate salt stress by altering their protein profile, i.e., salt-tolerant cultivars often express critical proteins more efficiently than salt-sensitive plants (Dissanayake et al., 2022), which shows that the quality of proteins is more important than quantity. Under salt stress, proteins including osmotin (N. tabacum) and gramin (O. sativa) play a vital role in maintaining cellular activities, while Na⁺ ion toxicity is alleviated by heat shock proteins (HSPs) and late embryonic abundant (LEA) proteins (Chourey et al., 2003; Derevyanchuk et al., 2016; Kumar et al., 2022). Despite the challenges in classifying cell wall proteins due to their diverse functions, recent classification has identified various categories, including those involved in metabolism, signaling, and structure (such as extensins, cellulose synthases, and pectin-modifying enzymes). Understanding the complex interplay of these proteins in stress perception and response is crucial for developing resilient crop varieties, as ongoing research seeks to explore the precise mechanisms by which the CWPs facilitate plant adaptation to environmental challenges.

Reactive oxygen species (ROS) are oxygen-derived molecules that function as both essential signaling mediators and potential inducers of cellular damage under stress conditions. The major forms of ROS include superoxide anion (·O₂ ^-), hydrogen peroxide (H₂O₂), hydroxyl radical (·OH), and singlet oxygen (¹O₂). Salinity triggers osmotic, ionic, and oxidative stress in plants (van Zelm et al., 2020). Initially, osmotic stress caused by decreasing water supply reduces cellular turgor, impacting cell expansion and tissue retraction. To retain cell integrity, plants actively adjust their cell walls to reinforce structure and restore osmotic potential (Zonia and Munnik, 2007). Mutants with impaired cell wall biosynthesis, such as cesa6 and mur4, display pronounced growth inhibition under salt stress, underscoring the essential role of CWI in maintaining structural resilience and enabling adaptive responses to salinity (Zhang et al., 2016a; Zhao et al., 2020). Excessive Na⁺ accumulation causes ionic stress that disturbs enzymatic activity essential to metabolism and ion balance, which in turn affects the mechanical characteristics of cell walls, especially of pectin. Increased Na⁺ levels compete with Ca²⁺, disrupting pectin cross-linking, whereas salt stress activates pectin methyl esterases, affecting cell wall composition (Beauzamy et al., 2015; Gigli-Bisceglia et al., 2022). While ROS generated during salt stress can function as secondary messengers that allow peroxidases to remodel cell walls, excessive accumulation of ROS can cause oxidative damage and even plant death (Ma et al., 2012; Tenhaken, 2014). Thus, maintaining a balance of ROS levels is critical for plant survival in saline conditions. Mutants with deficient ROS regulation have revealed a complex relationship between plant ROS homeostasis, cell wall dynamics, and salt stress (Hong et al., 2020; Zhou et al., 2021). The synthesis of ROS during salt stress has both positive and negative impacts on plant growth. While high ROS can lead to oxidative damage and compromise cell integrity, low ROS can promote stress tolerance and cell wall remodeling (Liu et al., 2012). The balance between ROS generation and scavenging is crucial for maintaining CWI. Mutants with decreased ROS scavenging systems exhibit increased sensitivity to salinity (Hazman et al., 2015). Enzymes such as SOD and peroxidases help regulate oxidative stress. Furthermore, ROS-induced post-translational changes of cell wall components may influence the mechanical characteristics of the cell wall, influencing plant resilience under salt stress (Karkonen and Kuchitsu, 2015).

Plant with decreased anisotropic growth under salt stress contain disrupted cellulose assembly and microtubule dynamics. Salt stress changes the dynamics of CSCs and microtubules in Arabidopsis, resulting in the removal of CesAs from the plasma membrane and microtubule depolymerization quickly after salt exposure (Komis et al., 2002; Wang et al., 2007; Gutierrez et al., 2009; Crowell et al., 2010). Moreover, the actin cytoskeleton significantly contributes to plant responses under salt stress, influencing cellulose synthase distribution and overall cell wall organization. However, after several hours of restoration of non-saline condition, microtubules reassemble and CesAs return to the membrane, indicating that plants possess adaptive mechanisms for cellulose synthesis during recovery from salt stress (Wang et al., 2007; Endler et al., 2015). The recovery of microtubule organization during salt stress depends on critical proteins like CC1 and CC2, which are essential components of CSCs. Mutants deprived of proper functioning of these proteins exhibit decreased growth, particularly in saline environments (Endler et al., 2015). Salt tolerance and CC1 function are impaired when microtubule-binding motifs are disrupted, as this prevents proper interaction between CC1 and microtubules, hindering cellular processes essential for stress adaptation (Kesten et al., 2022). While there is no direct animal tau protein homolog in plants, similarities in microtubule-binding properties suggest that plant proteins, such as CC1, may perform a similar role in regulating microtubule dynamics. Tau proteins in animals stabilize microtubules by binding to them, and it is hypothesized that salt stress might affect CC1, possibly through phosphorylation. This modification could alter the interaction between CC1 and microtubules, thereby impacting microtubule stability and cellular processes crucial for the plant’s response to salt stress (Mietelska-Porowska et al., 2014). Another key component of the CSC is KOR1, an endoglucanase found in the CSC that is internalized during salt stress and contribute to cellulose production (Nagashima et al., 2020). However, more research on KOR1 trafficking is needed, as pharmacological agents such as phenylarsine oxide and 1-butanol used to deduce its function also affect broader signaling pathways and may not specifically target KOR1 trafficking (McLoughlin et al., 2013; Gujas et al., 2017). Interestingly, phosphatidic acid (PA), associated with resistance to salt stress, functions in cellular signaling and may impact the localization of KOR1 (Zhang et al., 2012). Understanding this interaction is critical for determining plant responses to salt stress and controlling cellulose production.

Salt stress significantly disrupts cytoskeletal organization, which in turn affects CWI and plant tolerance mechanisms. Microtubule dynamics, in particular, are crucial in coordinating cellular responses to salinity. Chemical inhibitors like oryzalin (a microtubule depolymerizer) and taxol (a stabilizer) have been shown to markedly influence plant salt tolerance (Wang et al., 2007). Microtubule stability is maintained by proteins like MAP65-1, which enhances microtubule bundling, and its loss of function increases vulnerability to salt stress (Zhang et al., 2012). PA produced by phospholipase D, not only activates MAP65–1 but also interacts with MPK6, together contributing to microtubule organization and salt tolerance (Zhou et al., 2017). MPK6 further coordinates salt stress responses by linking cytoskeletal stability to broader signaling networks, including the SOS pathway (Yu et al., 2010). Additional microtubule-associated proteins, such as RIC1, facilitate microtubule reassembly after salt-induced disruption, while recently identified tropomyosin-like (TTL) proteins stabilize microtubules and interact with the CSC, directly linking cytoskeleton dynamics to cell wall biosynthesis and stress resilience (Kesten et al., 2022). Actin filaments are also critical, with salt stress-induced expression of actin depolymerizing factor 1 (ADF1) supporting filament remodeling, and loss of ADF1 leading to defective actin organization and reduced seedling survival (Wang et al., 2021a). These cytoskeletal adjustments are tightly integrated with CWI sensing, which relies on plasma membrane-localized receptors such as FER and other RLKs that detect wall perturbations and trigger Ca²⁺ influx during salt stress (Jose et al., 2020). The interaction of signaling modules like LRX3/4/5 with RALFs further highlights the complexity of CWI perception and its regulation under stress (Zhao et al., 2018). While these studies advance our understanding of the cytoskeleton–cell wall interface in salinity responses, the downstream intracellular signaling pathways, particularly those centered on MPK6, remain poorly understood. Elucidating these pathways will be key to developing targeted strategies for improving salt tolerance in crops.

The interplay between the cytoskeleton and CWI is crucial for plant adaptation to salt stress. Microtubule dynamics are linked to cellulose synthesis, while actin filaments also contribute to cell wall organization. Salt stress affects the organization and stability of both cytoskeletal components, leading to altered cell wall properties. For instance, ADF influences the distribution of CSC, and its expression is modulated by salt stress (Crowell et al., 2010; Wang et al., 2021a). The coordination between microtubules and actin is essential for maintaining cell shape and growth under saline conditions, highlighting the importance of cytoskeletal regulation in stress responses.

In plant cells, the cell wall and plasma membrane are kept intact through turgor pressure. The gap between them is filled with plasma membrane proteins such as Arabinogalactan proteins (AGPs), Wall-Associated Kinases (WAKs), Fasciclin-like arabinogalactan proteins (FLAs), and CesA complexes. These proteins maintain the delicate balance between cell wall extensibility and turgor pressure. This balance is critical for plant cell growth, development, and division, ensuring that plants can grow and adapt to their environments. Thus, the interaction of these components is vital to the life cycle of a plant, driving its growth and structural integrity (Wolf and Greiner, 2012; Watanabe et al., 2015).

PME plays a significant role in cell wall extensibility and remodeling. It actively contributes to the loosening of the cell wall through the action of polygalacturonase, which degrades HG. This process is ultimately essential for cell adhesion and defense responses in plants. PME modifies the ionic content, cellular adhesion, and pH of plants under stress, influencing development through a mechanism called “acid growth” (Pelloux et al., 2007). Cell expansion and cell wall synthesis include four major processes, which are outlined in the review of Wolf and Greiner (2012). ROS are released when the cell wall senses changes. As a result of internal turgor pressure, the cell wall deforms, hydrates, and relaxes, and eventually, secretes new wall material. Cell wall extension in plants is primarily regulated by several key hormones. ROS are important players in cell wall development, as discussed by Karkonen and Kuchitsu (2015) ( Figure 2 ). In the context of the cell wall, ROS act as agents that help with loosening and signaling various biological processes. They are produced by several enzymes (NADPH oxidases, quinone reductases, amine oxidases, lipoxygenases, oxalate oxidases, class III peroxidases), while various scavenger enzymes balance ROS levels, which is crucial for plant health. Auxin, a key plant hormone, promotes cell elongation by encouraging wall stretching and modification (Majda and Robert, 2018). However, when the cell wall stops expanding, it becomes rigid. This rigidity is due to the formation of strong connections known as di- and higher oligomer bridges, which are tightened further by ferulate coupling (Fry, 2004; Harris and Trethewey, 2009). H₂O₂ also contributes to this process, as it can inhibit cell wall growth through certain crosslinking reactions (Cona et al., 2006).

The cytoskeleton and associated proteins also play a critical role during plant cell division. Microtubule and actin filament structures are essential for this process, facilitating the synthesis of new cell walls through a specialized structure called the phragmoplast, which directs vesicles during cell division (Rasmussen et al., 2013). When plants face elevated salinity stress, they must adapt quickly to ensure proper cell expansion and resource utilization. Salt stress can lead to overaccumulation of Na⁺, causing K⁺ to efflux and increase ROS levels. This imbalance can lead to oxidative damage, disrupting turgor pressure and osmotic stability within the cells (Krasensky and Jonak, 2012; Zhang and Shi, 2013). One key player in this response is the CesA enzyme, which regulates cellulose synthesis to help manage the challenges posed by salt stress (Wang et al., 2016). Salt stress also destabilizes (depolymerizes) the microtubular structures of cells, causing CesA complexes in the membrane to become internalized (Paredez et al., 2006). A proposed model in which the CC protein interacts with microtubules and CesAs to maintain cellulose production and support plant growth during salt stress (Endler et al., 2015). BR, a class of plant hormones, also plays a vital role in this process. BR signaling may influence cell wall remodeling by regulating genes and enzymatic activities related to cell walls, particularly in grasses under stress (Rao and Dixon, 2017).

Additionally, proteins like RSA/MUR3/KAM1 help maintain the organization of actin microfilaments, enhancing salt tolerance by reducing ROS-induced damage (Li et al., 2013). During stress conditions, peroxidases utilize ROS in the apoplast to catalyze the cross-linking of phenolic compounds and glycoproteins in the cell wall, which helps to strengthen the wall and improve stress tolerance. This interaction reduces cell wall extensibility and limits cell expansion (Tenhaken, 2014). Interestingly, with prolonged salt exposure, cell wall extensibility can increase due to higher concentrations of ROS, specifically hydroxyl radicals. Enzymes such as xyloglucan-modifying enzymes and expansins in the apoplast can cleave glycosidic bonds in the cell wall, facilitating growth recovery (Tenhaken, 2014). Furthermore, the FER protein is essential for sensing salt stress and aiding cell recovery. In the absence of FER, cells may burst during recovery. It is believed that Na⁺ ions disrupt Ca²⁺ pectin cross-links in the cell wall, but FER helps balance Ca²⁺ levels by promoting cytosolic calcium, which is crucial for growth recovery (Feng et al., 2018). Understanding how these hormones and cellular mechanisms interact during salt stress can provide insights into enhancing plant resilience and improving agricultural practices (Mao et al., 2023).

The plant cuticle is primarily composed of cutin and waxes, forms a lipid-rich barrier over epidermal cell walls and plays a critical role in stress adaptation. Unlike the polysaccharide matrix of the inner wall, cuticular deposition is uniquely positioned to regulate non-stomatal water loss, ion exclusion, and mechanical protection traits vital under salt stress. Salt stress has been shown to induce transcriptional reprogramming of cuticle biosynthesis genes. For instance, studies in Arabidopsis thaliana and rice have demonstrated that salinity upregulates genes such as WIN1/SHN1, CER1, LACS2, and WSD1, which are involved in wax synthesis, transport, and polymerization (Liu et al., 2019; Tiika et al., 2025). Enhanced wax deposition under salinity improves leaf surface hydrophobicity and reduces passive ion influx, thereby contributing to ionic homeostasis.

Similarly, cutin biosynthesis is altered during salt exposure. The expression of genes such as GPAT6, CYP86A2, and LCR is responsive to salinity and modulates the ester-linked polyester matrix of the cuticle. Overexpression of GPAT6 in Solanum lycopersicum was found to enhance both cutin monomer levels and salt stress tolerance by maintaining water potential and delaying ion toxicity (Petit et al., 2016). In addition to structural roles, cuticle-derived signals, such as fatty acid precursors and long-chain aldehydes, activate downstream ABA-dependent pathways or interact with ROS signaling, thereby integrating surface defense with internal stress responses (Lü et al., 2009). Collectively, these findings suggest that cuticle reinforcement through wax and cutin deposition is a critical but often underappreciated component of the plant’s salt stress response. By limiting water loss and serving as a biochemical shield, the epidermal barrier enhances plant survivability in saline environments. Incorporating cuticle modifications alongside cell wall remodeling provides a comprehensive understanding of plant surface adaptations to abiotic stress.