The Dynamic Remodeling of Plant Cell Wall in Response to Heat Stress

Abstract

Heat stress has a significant negative impact on plant growth, development, and yield. The cell wall, a key structural feature that sets plants apart from animals, not only acts as the first physical barrier against heat stress but also plays an active role in the heat stress (HS) response through signaling pathways. The plant cell wall has a complex structural composition, including cellulose, hemicellulose, lignin, and pectin. These components not only provide mechanical support for cell growth but also constitute the material basis for plant response to environmental changes. This review summarizes recent research on how the cell wall's structural composition affects its mechanical properties in response to stresses. It examines changes in plant cell walls under HS and the adaptive mechanisms leading to cell wall thickening. Additionally, it explores the role of cell wall integrity in sensing and transmitting HS, along with the molecular mechanisms that maintain this integrity. Finally, it addresses unresolved scientific questions regarding plant cell wall responses to HS. This review aims to provide a theoretical foundation and research direction for enhancing plant thermotolerance through genetic improvement of the cell wall.

Keywords: cell wall; cell wall integrity; cellulose; heat stress; pectin.

Figure 1

Mechanisms of plant cell wall remodeling in response to heat stress. During the initial HS perception phase, the contents of cellulose, hemicellulose, and lignin decrease, and pectin methylesterification is reduced by activating pectin methylesterase (PME) activity. These modifications serve dual physiological functions: they facilitate cell wall thinning and cellular expansion, promoting an increase in cytoplasmic Ca²⁺ concentration as an immediate adaptive response to elevated temperatures; simultaneously, they compromise cell wall integrity (CWI), leading to the generation of damage-associated signals. These signaling molecules are recognized by plasma membrane-localized receptors, triggering calcium-dependent signaling cascades that activate the expression of heat-responsive genes including transcription factors and heat shock proteins. Concurrently, HS initiates a transcriptional reprogramming that upregulates cellulose synthase genes (ZmCESA2), hemicellulose-modifying enzymes (ZmHSL and XTH), and lignin biosynthesis genes (TaPAL33 and OsCCR17). This transcriptional response is coordinated with post-translational regulation involving suppression of PME activity and activation of pectin methylesterase inhibitors (PMEI). Collectively, these molecular adjustments lead to increased deposition of cellulose, hemicellulose, and lignin, elevated pectin methylesterification, subsequent cell wall thickening, and enhanced mechanical strength and thermotolerance. CWI: cell wall integrity; H₂O₂: hydrogen peroxide; ROS: reactive oxygen species; NO: nitric oxide; CNGCs: cyclic nucleotide-gated channels; CaM: calmodulin; LLGs: glycosylphosphatidylinositol-anchored proteins; FER: FERONIA (a member of the CrRLK1L receptor kinase family); THE1: THESEUS1 (a member of the CrRLK1L receptor kinase family); CSC: cellulose synthase complex; WAKs: wall-associated kinases; LRX: leucine-rich repeat extensins; RALF: rapid alkalinization factor; HSF: heat shock transcription factor; PMEs: pectin methylesterases; PMEI: pectin methylesterase inhibitor; XTHs: xyloglucan endotransglucosylase/hydrolase; TaPAL33: Triticum aestivum phenylalanine ammonia-lyase 33; OsCCR17: Oryza sativa cinnamoyl-CoA reductase 17. This figure was created by a online website BioRender. https://BioRender.com/633o967 (accessed on 22 May 2025).