Salt stress is a major environmental stress that affects plant growth and development. Plants are sessile and thus have to develop suitable mechanisms to adapt to high-salt environments. Salt stress increases the intracellular osmotic pressure and can cause the accumulation of sodium to toxic levels. Thus, in response to salt stress signals, plants adapt via various mechanisms, including regulating ion homeostasis, activating the osmotic stress pathway, mediating plant hormone signaling, and regulating cytoskeleton dynamics and the cell wall composition. Unraveling the mechanisms underlying these physiological and biochemical responses to salt stress could provide valuable strategies to improve agricultural crop yields. In this review, we summarize recent developments in our understanding of the regulation of plant salt stress.

The opening and closing of stomata are crucial for plant photosynthesis and transpiration. Actin filaments undergo dynamic reorganization during stomatal closure, but the underlying mechanism for this cytoskeletal reorganization remains largely unclear. In this study, we identified and characterized Arabidopsis thaliana casein kinase 1-like protein 2 (CKL2), which responds to abscisic acid (ABA) treatment and participates in ABA- and drought-induced stomatal closure. Although CKL2 does not bind to actin filaments directly and has no effect on actin assembly in vitro, it colocalizes with and stabilizes actin filaments in guard cells. Further investigation revealed that CKL2 physically interacts with and phosphorylates actin depolymerizing factor 4 (ADF4) and inhibits its activity in actin filament disassembly. During ABA-induced stomatal closure, deletion of CKL2 in Arabidopsis alters actin reorganization in stomata and renders stomatal closure less sensitive to ABA, whereas deletion of ADF4 impairs the disassembly of actin filaments and causes stomatal closure to be more sensitive to ABA. Deletion of ADF4 in the ckl2 mutant partially recues its ABA-insensitive stomatal closure phenotype. Moreover, Arabidopsis ADFs from subclass I are targets of CKL2 in vitro. Thus, our results suggest that CKL2 regulates actin filament reorganization and stomatal closure mainly through phosphorylation of ADF.

Stomatal movement is critical for plant responses to environmental changes and is regulated by the important signaling molecule phosphatidylinositol 3-phosphate (PI3P). However, the molecular mechanism underlying this process is not well understood. In this study, we show that PI3P binds to stomatal closure-related actin-binding protein1 (SCAB1), a plant-specific F-actin-binding and -bundling protein, and inhibits the oligomerization of SCAB1 to regulate its activity on F-actin in guard cells during stomatal closure in Arabidopsis thaliana. SCAB1 binds specifically to PI3P, but not to other phosphoinositides. Treatment with wortmannin, an inhibitor of phosphoinositide kinase that generates PI3P, leads to an increase of the intermolecular interaction and oligomerization of SCAB1, stabilization of F-actin, and retardation of F-actin reorganization during abscisic acid (ABA)-induced stomatal closure. When the binding activity of SCAB1 to PI3P is abolished, the mutated proteins do not rescue the stability and realignment of F-actin regulated by SCAB1 and the stomatal closure in the scab1 mutant. The expression of PI3P biosynthesis genes is consistently induced when the plants are exposed to drought and ABA treatments. Furthermore, the binding of PI3P to SCAB1 is also required for vacuolar remodeling during stomatal closure. Our results illustrate a PI3P-regulated pathway during ABA-induced stomatal closure, which involves the mediation of SCAB1 activity in F-actin reorganization.

Salt stress is a major challenge to agricultural productivity and can adversely affect plant growth and development. This review examines the interaction between cell wall architecture and plant tolerance to salt stress, focusing on the mechanisms underlying growth, remodeling, and anisotropic morphogenesis. It further elucidates how the cell wall’s composition, structure, and mechanical properties affect osmotic balance, ion transport, and physiological responses to salinity in plants. Key strategies for adaptation to stress, including the synthesis of osmoprotectants and alterations in cell wall polysaccharides, are discussed to understand their role in cell integrity and expansion under salt conditions. In addition, the review emphasizes the dynamic remodeling of the cell wall, which promotes anisotropic growth patterns necessary to maintain plant structure and function under environmental stresses. Based on the current research, this review highlights potential pathways to enhance plant adaptation to salinity through targeted manipulation of cell wall properties, providing insights for future biotechnological applications to improve crop performance in a saline environment.

Very-long-chain fatty acids (VLCFAs) are precursors for the synthesis of various lipids, such as triacylglycerols, sphingolipids, cuticular waxes, and suberin monomers, which play important roles in plant growth and stress responses. However, the underlying molecular mechanism regulating VLCFAs’ biosynthesis in quinoa (Chenopodium quinoa Willd.) remains unclear. In this study, we identified and functionally characterized putative 3-ketoacyl-CoA synthases (KCSs) from quinoa. Among these KCS genes, CqKCS2B.1 showed high transcript levels in the root tissues and these were rapidly induced by salt stress. CqKCS2B.1 was localized to the endoplasmic reticulum. Overexpression of CqKCS2B.1 in Arabidopsis resulted in significantly longer primary roots and more lateral roots. Ectopic expression of CqKCS2B.1 in Arabidopsis promoted the accumulation of suberin monomers. The occurrence of VLCFAs with C22–C24 chain lengths in the overexpression lines suggested that CqKCS2B.1 plays an important role in the elongation of VLCFAs from C20 to C24. The transgenic lines of overexpressed CqKCS2B.1 showed increased salt tolerance, as indicated by an increased germination rate and improved plant growth and survival under salt stress. These findings highlight the significant role of CqKCS2B.1 in VLCFAs’ production, thereby regulating suberin biosynthesis and responses to salt stress. CqKCS2B.1 could be utilized as a candidate gene locus to breed superior, stress-tolerant quinoa cultivars.