Integrative dynamics of cell wall architecture and plant growth under salt stress

Abstract

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.

Keywords: cell growth; cell wall composition; cell wall integrity; plant cell anisotropy; salt stress.

Figure 1

Overview of the effects of salt stress on plant cell wall integrity, loosening, and component biosynthesis. Salt stress in plants triggers both osmotic and oxidative stress, resulting in impaired water uptake and excessive generation of reactive oxygen species (ROS). These ROS contribute to structural damage and destabilization of matrix polysaccharides, ultimately inhibiting cell wall loosening and radial expansion. Consequently, the biosynthesis and stability of major wall components are adversely affected: cellulose becomes weakened, hemicellulose synthesis is disrupted, pectin is degraded, and lignin biosynthesis is suppressed. The intracellular sugar metabolism and biosynthetic pathways contributing to the formation of cellulose, hemicellulose, and pectin. Red-labeled genes and enzymes represent transcriptional or post-transcriptional upregulation under salt stress, including transcription factors (MYB46, SND1, NAC1, NAC16, HSFA7b, EIL2, MYB3) and key biosynthetic enzymes (UGE3, UGD, UGP, UXS, GMD, GER, GAE), which drive stress-induced remodeling of cell wall metabolism. Under normal conditions (left panel), cell wall-loosening enzymes such as XTHs and expansins facilitate expansion and growth, while salt stress (right panel) disrupts these processes, leading to reduced wall plasticity and stunted plant development. The figure integrates metabolic, transcriptional, and biophysical responses, providing a comprehensive view of how salt stress alters plant cell wall dynamics and growth.

Figure 2

Cellular mechanisms of plant cell wall growth and extensibility under salt stress. This schematic illustrates how salt stress impairs cell wall extensibility by disrupting CWI, microtubule dynamics, ion balance, and calcium-pectin interactions, while also outlining mechanisms of recovery. (1) Under optimal conditions, key structural and signaling proteins such as AGPs, WAKs, FLAs protein, and CesAs, coordinate cell wall deposition and expansion, maintaining mechanical stability and enabling anisotropic growth. (2) PME modifies homogalacturonan domains, enhancing wall plasticity and promoting cell elongation. (3) Salt-induced ionic stress (notably Na⁺ influx) triggers cortical microtubule depolymerization, which impairs CesA trafficking and cellulose synthesis, compromising wall stiffness and directional expansion. (4) Upon stress alleviation, the receptor-like kinase FER modulates calcium–pectin cross-linking, restoring wall elasticity and supporting structural repair. Importantly, proteins such as FEI1/FEI2, MIK2, and FORMIN act as mechanosensors and regulators that bridge cytoskeletal organization with CWI maintenance, playing essential roles in signal transduction and cytoskeleton–cell wall coupling under salinity stress. These components collectively enable plants to perceive wall damage, transduce stress signals, and initiate adaptive remodeling responses crucial for survival in saline environments.

Figure 3

Mechanisms of anisotropic growth during salt stress in plants. (A) Under normal conditions, the cell wall cellulose and hemicellulose network support anisotropic growth, where cells elongate in a specific direction. In contrast, salt stress alters the orientation of cellulose fibers, resulting in isotropic growth, where cell expansion becomes less directional and more uniform across all axes. (B) Salt stress leads to an imbalance in ion homeostasis, with Na⁺ and K⁺ ions accumulating within the cell, disrupting the membrane’s integrity, and generating ROS. These ROS damage cell membranes and internal structures, inhibiting normal growth and causing cellular dysfunction. (C) The FER receptor plays a critical role in maintaining cell wall integrity during salt stress. FER interacts with extracellular signals and regulates ion homeostasis, helping to prevent excessive damage to the cell wall. By balancing Ca²⁺ and Cl^- levels, FER prevents premature cell bursting and supports anisotropic growth under stress. (D) Expansins are key enzymes in loosening the cell wall, enabling recovery after salt stress. They interact with pectin and cellulose components to relax the wall, facilitating cell expansion. The reorganization of microtubules and cellulose fibers, coupled with expansin activity, helps restore anisotropic growth patterns, allowing plants to adapt and recover from salt-induced growth inhibition.