The process of cellulose biosynthesis is complex and tightly regulated, and it is interrupted by salt stress on multiple levels and resulted in growth defects/inhibition, anatomical abnormalities, and hypersensitivity to salt stress. Several transcription factors, epigenetic regulatory mechanisms, and hormones, have been shown to affect the cellulose biosynthesis process upon salt stress perception ( Table 1 ). However, salt-mediated modulation of the cellulose biosynthesis process should be always considered in close association with other metabolic and physiological responses caused by salt stress. Further investigation and understanding of the exact molecular mechanisms of every cellulose biosynthesis-associated genes/proteins involved in salt stress tolerance development would promote its practical application in creating salt-tolerant varieties of different plant species.

Cellulose micro-fibrils are β-1,4 linked glucose polymer that is synthesised at the cell surface by cellulose synthase (CesA) complexes (CSCs) not only by higher plants but also algae, some bacteria and even animals, thus, making it the most abundant polymer on the planet (Allen et al., 2021). CesAs are the key part of CSCs, which are active only in the plasma membrane, while actively communicating with the Golgi apparatus and other intracellular compartments via exocytosis (trafficking to the plasma membrane) and endocytosis (removal from the plasma membrane). Microtubules and actin microfilaments serve as tracks along which motor proteins transport cell wall components in vesicles. The direct interactions between microtubules, microtubule-linking proteins, and cellulose synthases made the proper microtubules and microfilaments organisation critical for the positioning and construction of cell wall components (Colin et al., 2023). At the same time, the genes in CesA family are specialised, with CesA1, CesA3, and CesA6 participating in primary cell wall synthesis, while CesA4, CesA7, and CesA8 are involved in secondary cell wall synthesis. Also, some other proteins, such as CSI1 (cellulose synthase–interacting protein 1) and CC1-2 (companion of cellulose synthase 1 and 2), are also required for cellulose biosynthesis (Zhu and McFarlane, 2022). Another recently identified members of the CSC are TTL (tetratricopeptide thioredoxin-like) proteins, which interact with CesA1 and cortical microtubules to promote their polymerisation, thus maintaining cellulose synthesis under salt stress conditions (Kesten et al., 2022).

Experimental data from the model plant Arabidopsis thaliana [(L.) Heynh.] demonstrated that cesA1 and cesA6 single mutants are salt sensitive, with severe root tip swelling, reduced cellulose contents, and root elongation. Mutant lines of csi1, which are known to directly interact with CesA6 and cortical microtubules, are also hyper-sensitive to salt stress (Zhang et al., 2016). Similarly, to Arabidopsis, RNAi knockdowns of CesA1 and CesA6 in broccoli (Brassica oleracea L.) resulted in anatomical and ultrastructural changes in leaves and chloroplasts, dwarf phenotype, and reduced content of the cellulose and pectins (40% and 19%, respectively). However, mutant plants had higher soluble sugar content and three times higher proline content compared with control plants. Furthermore, mutants have higher salt-stress resistance, which was associated with six to seven times up-regulated expression of salt-tolerance–related aquaporins PIP2;2 and PIP2;3 (Li et al., 2017). Thus, these genes might play the role of the negative regulator in plant osmoprotection.

CC1 and 2 proteins could interact with CESAs and microtubules and promote microtubule formation and dynamics. Mutations of the CC1 and 2 resulted in salt-sensitive phenotypes with altered microtubule and CSC behaviour in vivo. Under salt, stress CSCs are quickly dissociated from the plasma membrane, and functional CC proteins are necessary to maintain CesA migration and microtubule stability to reassemble CSCs during the growth recovery phase after salt treatment ( Figure 1B ) (Endler et al., 2015). Interestingly, plant CC1 implements an evolutionally conserved microtubule-binding mechanism, similar to that of Tau protein, which is associated with Alzheimer’s disease and known to self-aggregate and trigger neurodegeneration. In particular, two tyrosine residues in the N-terminal region of CC1 are responsible for the microtubule binding, both in vitro and in vivo. Point mutations in these residues interrupted normal microtubule-guided CSC movement and resulted in the generation of a salt stress-hyper-sensitive microtubule array (Kesten et al., 2019).

Recently, an ubiquitously expressed and salt-stress induced gene UGE3 (UDP-galactose/glucose epimerase 3) from rice, which provides substrates for polysaccharides polymerization, was demonstrated to improve biomass production, mechanical properties of the cell wall, and increased tolerance to salt and osmotic stresses. uge3 mutants displayed diverse growth defects and were hypersensitive to osmotic and salt stresses. On the other side, OsUGE3 overexpressing plants had increased biosynthesis of cellulose and hemicelluloses, which resulted in improved mechanical strength of the cell wall. Furthermore, OsUGE3 overexpressors showed increased tolerance to osmotic and salt stresses, which was associated with improved Na⁺ and K⁺ homeostasis and higher accumulation of soluble sugars (Tang et al., 2022).

Additionally, some other cellulose biosynthesis-related proteins have also been reported involved in salt tolerance. For example, KORRIGAN1 (KOR1), a membrane-anchored endo-β-1,4-glucanase, is an integral part of the primary cell wall, physically interacting with CSC and linking cell wall biosynthesis and abiotic stress tolerance. KOR1 was shown to cycle between the trans-Golgi network and the plasma membrane under normal conditions. While under salt stress, this cycling is interrupted, and KOR1 is retained in the plasma membrane or transported to the tonoplast for degradation, thus unable to support cellulose biosynthesis. Not surprisingly, kor1 mutants have the salt-stress sensitive phenotype, cellulose deficiency, and retarded growth (Nagashima et al., 2020).

Recently, several mechanisms regulating cellulose biosynthesis in relation to salt-stress tolerance have been identified ( Figure 3 ). For example, overexpression of the NAC1 TF (transcription factor) in Switchgrass (Panicum virgatum L.) leads to higher cellulose content, enhanced tolerance to salt stress, and up-regulated expression of antioxidant defence and ion-homeostasis–related genes, reduced accumulation of Na⁺ and increased of K⁺ in roots and shoots. At the same time, NAC1 RNAi plants were hyper-sensitive to salt stress (Wang et al., 2019b). Arabidopsis AtHSFA7b [heat shock factor (class A)–type transcription factor], known to participate in abiotic stress responses, is also involved in salt tolerance. Under salt conditions, AtHSFA7b improved salt tolerance by regulating genes, such as SOS1, NHXs, PODs (peroxidase), and SODs (superoxide dismutase). These gene interactions lead to the reduction of water loss rate, adjustment of osmotic potential, and a decrease in the accumulation of reactive oxygen species. In particular, the content of proline and soluble sugars was increased after NaCl treatment in an AtHSFA7b-dependent way. Under salt-stress conditions, plant lines overexpressing AtHSFA7b had increased levels of proline biosynthesis genes (AtP5CS1 and AtP5CS2, encoding Δ1-pyrroline-5-carboxylate synthases), while hstfa7b plants had lower AtP5CS1 and AtP5CS2 expression. Several other TFs, positive regulators of salt stress, were regulated by AtHSFA7b: bHLH, NAC061, NAC036, NAC090, WRKY38, and ZFP2 (Zinc finger protein). Finally, 31 cellulose biosynthesis-related genes [including CESA8, CSLG1 (cellulose synthase-like glycosyltransferase), CSLG2, and CSLA9] were down-regulated by AtHSFA7b, suggesting these genes as negative modulators of salt tolerance (Zang et al., 2019).

Epigenetic mechanisms also play an important role in salt tolerance. As it was recently demonstrated, the mRNA levels of histone acetyltransferase GCN5 (general control non-repressed protein 5) were increased after salt treatment, thus suggesting its importance in maintaining the cell wall integrity under salt stress. Several genes, such as CTL1 (chitinase-like gene), PGX3 (polygalacturonase involved in expansion 3), and MYB54 (MYB domain protein 54), involved in cellulose biosynthesis, were identified as direct GCN5 targets. Confirming these results, the gcn5 mutants exhibited reduced cellulose content, severe growth inhibition, and cell wall anomaly under salt stress. Furthermore, the salt tolerance and cell wall integrity phenotypes of the Arabidopsis gcn5 mutant were complemented by the expression of the wheat TaGCN5 gene, suggesting a conserved role of the GCN5-mediated salt tolerance between these two species (Zheng et al., 2019).

Additionally, the plant hormone ABA, known to regulate various aspects of plant growth, development, and stress responses, is also linked to cellulose synthesis-regulated salt stress tolerance. The rice OsCSLD4 (cellulose synthase-like D4 protein) mutant (nd1) was sensitive to salt stress but insensitive to ABA treatments. Interestingly, the expression of some ABA synthesis and signaling genes was repressed in nd1 mutant under both normal and salt stress conditions. Exogenous ABA treatment effectively complemented nd1 salt-stress sensitive phenotype. Furthermore, OsCSLD4 overexpression leads to the up-regulated expression of ABA biosynthesis genes, increased ABA content and enhanced rice salt-stress tolerance, suggesting that the role of OsCSLD4 in salt stress tolerance is ABA-mediated (Zhao et al., 2022).

Hemicelluloses are branched heteropolymer interacting and cross-linking cellulose microfibrils, thus strengthening plant cell walls (Khodayari et al., 2021). A recent study on vascular plants suggested that hemicelluloses could also interact with lignin in some cell walls (Gallina et al., 2018). The abundance and structure of hemicelluloses vary greatly in different plant species, with main examples grouped into xylan, xyloglucan, arabinoxylan, glucuronoxylan, and glucomannan (Scheller and Ulvskov, 2010). Xyloglucan is involved in cell wall strengthening via cellulose microfibrils binding during cell elongation, while xylan participates in polysaccharide cross-linking during cell wall architecture establishment. Modification of hemicelluloses by the cell wall remodelling enzymes is an important way to control cell wall extensibility, and XTHs (xyloglucan endotransglucosylase/hydrolases) is the best-studied family facilitating cell wall plasticity (Ishida and Yokoyama, 2022). XTHs can cleave and/or reconnect xyloglucans, which leads to the attachment of the reducing end of the xyloglucans to the non-reducing end of another xyloglucans, thus producing chimeric oligomer or polymer xyloglucan molecules (Park and Cosgrove, 2015). XTHs homologues react to salt stress differently, with some homologues up-regulated, while other – down-regulated and some did not change their level of expression. Therefore, further identification and detailed investigation of every XTHs’ (both positive and negative) regulator would help to create new plants with improved tolerance to salt stress.

Early research demonstrated that XTHs are active players in various abiotic stresses, including high-salinity stress. Experiments on Medicago truncatula demonstrated that XTHs responded differently to salt stress, with eight up-regulated and 11 down-regulated genes (Xuan et al., 2016). Similar results were reported also for poplar (Populus sp.), where 11 differently expressed genes were identified in the roots (five up- and six down-regulated), nine in the stems (four up- and five down-regulated), and seven in the leaves (four up- and three down-regulated) after salt treatment (Cheng et al., 2021). These data were confirmed on other species such as typical halophyte, Salicornia europaea, where salt stress up-regulated expression of 27 and 15 SeXTHs (in shoots and roots, respectively) (Tiika et al., 2021), and Vitis vinifera L., four VvXTHs were observed (Qiao et al., 2022). Therefore, XTHs’ expression is tissue specific, and some members of the family are positive regulators of salinity tolerance, while others are negative.

Thereby, transgenic tomato plants expressing pepper (Capsicum annuum L.) CaXTH3 demonstrated an increased tolerance for drought and salt stresses ( Table 1 ). Transgenic plants had normal phenotype under standard growth conditions and also no significant difference in chlorophyll content and root elongation under salt stress (Choi et al., 2011). Similarly, the expression of poplar (Populus euphratica Oliv.) PeXTH in tobacco improved water-retaining capacity and photosynthesis efficiency and increased the number of mesophyll cells under salt-stress conditions (Han et al., 2013). Transgenic Arabidopsis and tomato plants expressing persimmon (Diospyros kaki Thunb.) XTH had larger and more irregular cells with a higher density of cell walls and intercellular spaces, which resulted in enhanced tolerance for salt and drought stresses (Han et al., 2017).

A negative role in salt tolerance was reported for Arabidopsis XTH30, which was strongly up-regulated under salt stress in the stem, root, flower, and hypocotyl. However, plants overexpressing XTH30 were hyper-sensitive to salt stress, while loss-of-function XTH30 mutant demonstrated lower Na⁺ accumulation in shoot and H₂O₂ content and increased salt tolerance (Yan et al., 2019).

In addition to diverse abiotic stresses, the expression of XTH is regulated by plant hormones. For example, XTH from tobacco (Nicotiana tabacum L.) was up-regulated by both ABA treatment (10 μM) and different stresses (drought, salt, and cadmium), while down-regulated by higher ABA concentration (100 μM) and 0^°C stress, thus suggesting its implication in ABA-dependent stress signaling. At the same time, NtXTH overexpressing tobacco plants demonstrated a higher rate of root growth under salt-stress conditions, and also greater frost and heat tolerance when compared with control plants (Kuluev et al., 2017). In Arabidopsis, XTH19 and XTH23 were induced by salt stress via the brassinosteroid signaling TF BES1 (BRI1-EMS-SUPPRESSOR 1). xth23 single and xth19/xth23 double mutant were additively sensitive to salt stress, while BES1 overexpression increased salt tolerance in wild-type and partially complement salt tolerance and phenotype of xth19/xth23 mutant. Further experiments showed that XTH19 and XTH23 expression is directly regulated by BES1, thus postulating a novel role for brassinosteroids in regulating XTH-mediated salt sensitivity (Xu et al., 2020).

Pectins are acidic polysaccharides enriched with α-(1,4)–linked galacturonic acids and accounted for up to 40% of the higher plant cell wall content. Pectins play a crucial role in plant growth and development, immunity, response to stresses, and senescence [reviewed in (Cruz-Valderrama et al., 2019; De Lorenzo et al., 2019; Dauphin et al., 2022)]. The three major types of pectins are HG (homogalacturonan), RG-I (rhamnogalacturonan-I), and RG-II (rhamnogalacturonan-II), which are selectively modified by PMEs (pectin methyl esterases), PAEs (pectin acetylesterases), PGs (polygalacturonases), or PLLs (pectate lyases–like) during cell growth or in response to stresses. The dynamic regulation and interplay between expression and activity of modified enzymes and their inhibitors [such as PMEIs (PME inhibitors) and EGCG (epigallocatechin gallate)] define the extent of cell walls stiffness [reviewed in (Coculo and Lionetti, 2022)] (Du et al., 2022). Different pectin-modified enzymes have been shown to act as positive or negative regulators of salt tolerance in plants.

Thereby, in tobacco (Nicotiana tabacum L.) NtPME005, NtPME039, NtPME043, NtPME047, NtPME082, NtPME106, and NtPME108 were induced and up-regulated, while NtPME029, NtPME056, NtPME058, and NtPME062 were down-regulated by salt stress. Interestingly, some NtPME genes (NtPME005, NtPME039, and NtPME106) were down-regulated by ABA treatments and up-regulated by NaCl stress, suggesting the involvement of ABA pathway in salt stress tolerance (Sun et al., 2022). Expression PMEI1 from Chorispora bungeana (Fisch.) and its Arabidopsis homologue PMEI13 in Arabidopsis reduced PMEs tissue activity and increased salt tolerance. Interestingly, both CbPMEI1 and PMEI13 genes were repressed by salt stress and ABA treatments, thus further supporting the involvement of ABA in PME-mediated salt tolerance regulation (Chen et al., 2018).

Recently, another ABA-mediated mechanism of salt-stress tolerance was demonstrated on rice (Oryza sativa L.). In particular, OsEIL2 (EIN3-Like) (ETHYLENE-INSENSITIVE 3), a nuclear-localised TF induced by salt stress and ABA treatment, directly binds and regulates genes encoding β subunit of polygalacturonase subfamilies (OsBURP14 and OsBURP16) ( Table 1 ). OsEIL2 overexpression resulted in delayed leaf development, decreased (because of the increased PG activity) pectins content and reduced tolerance to salt and drought stresses. On the contrary, OsEIL2 RNAi knockdown mutant demonstrated delayed leaf senescence and enhanced tolerance to salt and drought stresses (Jin et al., 2020). Another conserved gene, DGR2 (DUF642 L-GALACTONO-1,4-LACTONE-RESPONSIVE) from Amaranthus hypochondriacus (L.), encoding DUF642 domain–containing protein induced by drought and salt stresses, was also associated with cell wall modifications. AhDGR2 overexpression in Arabidopsis led to hypersensitivity to NaCl and ABA, and general abiotic stress intolerance. Interestingly, the effect of AhDGR2 overexpression on the PMEs activity was organ-specific, significantly lower in leaves but higher in roots, thus suggesting further insights into the precise regulation of cell wall modifications (Palmeros-Suárez et al., 2017). Similarly, overexpression of tea [Camellia sinensis (L.) Kuntze] CsF3H gene, encoding flavanone 3-hydroxylase in tobacco, increased tolerance to salt stress via decreased PMEs activity in roots and leaves. Also, transgenic plants demonstrated reduced electrolyte leakage and MDA (malondialdehyde) levels, while increasing the content and activity of antioxidant enzymes (Mahajan and Yadav, 2014).

PMEs are novel and often overlooked players in the development of salt stress tolerance. PMEs are closely associated with ABA signaling pathways, a wide range of cell-surface sensors and other abiotic stresses-related genes. However, the exact regulatory circuit and molecular mechanism of their action are unknown and require further investigation.

Arabidopsis PME31 was significantly up-regulated after salt treatment. It was shown that PME31 acts as a positive regulator of salt stress tolerance. Accordingly, PME31 knockdown resulted in hypersensitivity to salt stress and down-regulation of other genes related to drought and temperature stresses [such as DREB2A (dehydration-responsive element-binding protein), RD29A (low-temperature–induced 78 kDa protein) and RD29B] (Yan et al., 2018). Similarly, the mutation in rice PME (OsTSD2) reduced the expression of several genes maintaining ion homeostasis (OsKAT1, OsSOS1, and OsHKT1), which resulted in increased accumulation of Na⁺ and a lower level of K⁺ in shoot under salt stress (Fang et al., 2019).

Additionally, cell walls perceive various stresses with cell-surface localised receptors, such as WAKs (wall-associated kinases), LyKs (LysM receptor-like kinases), LRR-RLKs (leucine-rich repeat receptor-like kinases), LRXs (Leucine-rich repeat extensins) and CrRLK1L (Catharanthus roseus receptor-like kinase 1-like) [reviewed in (Bacete et al., 2018)]. FERONIA (FER) is a plasma membrane–localised receptor kinase perceiving salt-stress–mediated damage to the pectins-associated wall. Therefore, root cells of fer mutant were shown to explode during growth recovery after salt treatment. Conducted in vitro experiments proposed a mechanism where FER directly interacts with pectins, senses salinity-mediated softening of the cell wall and initiates a Ca²⁺-mediated signaling cascade preventing root cells from exploding during growth under salt stress. The exposure to the salt stress causes the surplus of Na⁺ to replace Ca²⁺ in pectins binding, thus interrupting normal cross-linking of pectins and reducing cell elongation, Ca²⁺ or borate treatment could rescue fer-associated phenotype and facilitating pectins cross-linking (Feng et al., 2018). Later studies provide evidence of the close association between FER and LRX3/4/5 (Dünser et al., 2019), and RALF22/23 (RAPID ALKALINIZATION FACTOR) (Yu and Assmann, 2018), thus proposing their functioning as a LRX-RALF-FER module to transduce cell wall signals plant growth in normal condition and tolerance to salt stress ( Figure 1B ) (Zhao et al., 2018). Furthermore, recent research has identified that LRX-RALF-FER module regulates the homeostasis of jasmonic acid, salicylic acid and abscisic acid, thus controlling plant salt stress response (Zhao et al., 2021). Later, a similar mechanism was described for other sensors, such as THE1 (THESEUS1) and HERK1 (HERKULES1) (Gigli-Bisceglia et al., 2022), WAK2 [Brachypodium distachyon (L.) P.Beauv.], and AtWAK2 (Wu et al., 2020). In particular, while the1 and herk1 single mutants have wild-type salt stress phenotype, the double mutants have hypersensitive to salt stress phenotype, similar to fer mutants. In the proposed model THE-HERK sensors mitigated salt stress through the negative regulation of MAPK6 (mitogen-activated protein kinase 6) (Gigli-Bisceglia et al., 2022), which is known to regulate many cellular processes, including also salt stress response (Zhang and Zhang, 2022).

Lignin is the main structural component of the plant cell wall, composed of the units derived from the polymerisation of sinapyl, coniferyl, p-coumaryl, and hydroxycinnamyl alcohols ( Figure 4 ). Accumulation of lignin and cell wall thickening because of the activation of the lignin biosynthesis pathway is an important response to various environmental stresses, including high salinity [reviewed in (Vanholme et al., 2019; Coomey et al., 2020)].

The walls of specialised cells could be modified in response to salt stress, for example, the suberinisation of the endodermis and exodermis (hypodermis) (Shukla and Barberon, 2021). Such modifications affect the transfer of solutes and water, thus preventing the entrance of surplus Na⁺ and Cl^- into the plant and the leakage of K⁺ and water out (Byrt et al., 2018). TFs members of the MYB and WRKY families are the main regulators of suberin biosynthesis and deposition. Suberin metabolism is closely associated with other fatty acid-based pathways, such as cutin and wax biosynthesis.

Recently, MYB family TFs (MYB41, MYB53, MYB92, and MYB93) have been identified as the main regulators of suberin biosynthesis and deposition, each of which is sufficient to endodermal suberin formation in response to both environmental and developmental signals. Indeed, the quadruple mutant of these four TFs had greatly reduced levels of suberin and affected endodermal deposition of lignin (in CS), probably through a compensatory mechanism. Furthermore, mutant plants had increased sensitivity to salt stress and suberinisation, which was not regulated by ABA and salt treatments. Thus, supporting the central role of suberin in plant adaptation to salt stress (Shukla et al., 2021).

Similarly, MYB family TFs regulate suberin assembly also in the seed coat. As it was recently shown, seeds of myb9 and myb107 mutants demonstrated lower germination rates and increased permeability under salt stress due to the reduced amount of suberin monomers and changed levels of other seed coat-associated metabolites (Lashbrooke et al., 2016). Also, MYB49 was shown to contribute to salt-enhanced tolerance in Arabidopsis through the transcriptional activation of cutin deposition and antioxidant defence (Zhang et al., 2020). The plant cuticle, composed of cutin and associated waxes, is usually deposited on the surface of the epidermal cell wall of plant leaves and stems (Kosma et al., 2014). Cutin differs from suberin by lower phenolic content, almost exclusively C16 and C18 monomers, and around 50% of C18:2 monomers (Yang et al., 2017). Therefore, MYB49 overexpressing plants demonstrated significant up-regulation of the ‘cutin, suberin and wax biosyntheses’ category of genes under normal and/or salt stress conditions, while in myb49 mutants these genes were down-regulated. Several biosynthetic genes, such as ASFT (omega-hydroxypalmitate O-feruloyl transferase), FACT (fatty alcohol:caffeoyl-CoA acyltransferase), CYP86B1, which are crucial for incorporating aromatics into suberin, cutin and suberin-associated waxes, and TF MYB41, were defined as the direct targets of MYB49. Additionally, MYB49 overexpressing lines demonstrate improved antioxidant defence (peroxidases and LEA) and elevated Ca²⁺ levels in leaves, thus enhancing salt tolerance in plants (Zhang et al., 2020).

WRKY family TF 33 was recently identified as a crucial regulator of salt tolerance in both Arabidopsis and rice. Mutants of wrky33 and its direct target atcyp94b1 (involved in suberin biosynthesis) demonstrated reduced suberin content and salt-sensitive phenotype. However, AtCYP94B1 expressing plants in wrky33 background and rice wild-type improved both suberin content and salt tolerance, thus confirming the regulatory role of WRKY33 in CYP94B1-mediated salt-tolerance (Krishnamurthy et al., 2020). Similarly, AtWRKY9 was identified as a direct regulator of AtCYP86B1 and AtCYP94B3 responsible for salt stress tolerance. Atwrky9 mutant had reduced roots suberin content and reduced expression of AtCYP94B3 and AtCYP86B1. The salt-sensitive phenotype of atcyp94b3 and atcyp86b1 mutants was rescued by the expression of homologues genes from Avicennia officinalis (L.) AoCYP94B3 and AoCYP86B1 were also associated with reduced Na⁺ accumulation in the shoots (Krishnamurthy et al., 2021).

Suberin homeostasis is closely associated with fatty acid and carbohydrate metabolism. Similarly to other stress-related responses, ABA is involved in the suberin biosynthesis and deposition, CS formation and biosynthesis of compatible solute trehalose. However, the role of CS and CASPs family members requires further investigation.

Many individual genes involved in suberin biosynthesis have been demonstrated to improve the tolerance to salt stress. KCS (β-Ketoacyl-CoA synthase) catalyses the condensation of malonyl-CoA with acyl-CoA; thus, it is a crucial rate-limiting enzyme in the suberin biosynthesis (Rui et al., 2022). Expression of KCS11 from grape (Vitis vinifera L.) in Arabidopsis increased its salt-stress tolerance on germination and seedling stages. This improvement was mediated via several mechanisms: accumulation of osmotic regulating substances (increased proline content), membrane stabilisation (reduced MDA content), and normalisation of ions homeostasis (increased expression of genes encoding several ion transporters and channels (such as AKT1, CBLl9, CIPK23, SOS1, HKT1 and CHX14 (Cation/H(⁺) antiporter)) (Yang et al., 2020). Similarly, expression of KCS from quinoa (Chenopodium quinoa Willd.) in Arabidopsis increased the occurrence of VLFAs (very long-chain fatty acids) with C22-24 chain lengths and promoting the accumulation of suberin monomers, thus improving salt tolerance (Tariq et al., 2022). These results demonstrated that suberin plays rather a universal role in salt tolerance and suggested KCS family members as potential genes to improve the salt-stress tolerance in different species.

Recently, the role of CASPs (Casparian strip membrane domain proteins) in salt tolerance was demonstrated. CASPs (UPF0497) are required for the CS formation at the endodermis and regulation of the selective uptake of mineral elements by roots, in particular Si and Ca²⁺ (Wang et al., 2019). The expression of CASP4 from sorghum [Sorghum bicolor (L.) Mocnch] in Arabidopsis (in both WT and atcasp5 mutant) increased salt stress tolerance, which was associated with lower level osmotic stress-associated damages and Na⁺ accumulation in leaves. Furthermore, transgenic plants had longer roots and higher expression of the genes related to Casparian strip formation (Wei et al., 2021). However, experiments of CS defective mutants suggested that CS formation and suberin deposition processes are interrelated and closely regulated by endogenous factors [small secretory peptides, such as CIF (Casparian strip Integrity Factor) and environmental factors (availability of nutrients, abiotic stresses)] (Doblas et al., 2017). Therefore, further research is required to better understand the complex association between CASPs, lignin, and suberin deposition under the influence of salt stress and the application of different regulatory proteins.

Additionally, TPS (trehalose-6-phosphate synthase), which is required for the biosynthesis of compatible solute trehalose, which is a crucial osmoprotector during salt and drought stresses (Nuccio et al., 2015), also mediated enhanced suberin-associated salt tolerance. In particular, rice tps8 mutant demonstrated enhanced sensitivity to salt and ABA treatments, reduced content of soluble sugars, CS, and suberin deposition in the roots. In addition, ABA-responsive genes were down-regulated in tps8 plants. On the contrary, TPS8 overexpression rescued the salt-sensitivity associated phenotype and enhanced salt stress tolerance. These data suggested that rice TPS8 regulates salt tolerance via suberin deposition in an ABA-dependent way (Vishal et al., 2019). ABC family transporters (G type) are known to play a crucial role in suberin biosynthesis through the transport of suberin monomers from the cytoplasm to the apoplastic space (Shanmugarajah et al., 2019).