Summary: Plants have evolved a repertoire of monitoring systems to sense plant morphogenesis and to face environmental changes and threats caused by different attackers. These systems integrate different signals into overreaching triggering pathways which coordinate developmental and defence‐associated responses. The plant cell wall, a dynamic and complex structure surrounding every plant cell, has emerged recently as an essential component of plant monitoring systems, thus expanding its function as a passive defensive barrier. Plants have a dedicated mechanism for maintaining cell wall integrity (CWI) which comprises a diverse set of plasma membrane‐resident sensors and pattern recognition receptors (PRRs). The PRRs perceive plant‐derived ligands, such as peptides or wall glycans, known as damage‐associated molecular patterns (DAMPs). These DAMPs function as ‘danger’ alert signals activating DAMP‐triggered immunity (DTI), which shares signalling components and responses with the immune pathways triggered by non‐self microbe‐associated molecular patterns that mediate disease resistance. Alteration of CWI by impairment of the expression or activity of proteins involved in cell wall biosynthesis and/or remodelling, as occurs in some plant cell wall mutants, or by wall damage due to colonization by pathogens/pests, activates specific defensive and growth responses. Our current understanding of how these alterations of CWI are perceived by the wall monitoring systems is scarce and few plant sensors/PRRs and DAMPs have been characterized. The identification of these CWI sensors and PRR–DAMP pairs will help us to understand the immune functions of the wall monitoring system, and might allow the breeding of crop varieties and the design of agricultural strategies that would enhance crop disease resistance.

Significance: Plant cells are surrounded by an extracellular matrix known as the cell wall. We have analyzed the contribution of theArabidopsiscell wall to disease resistance to pathogens with different parasitic styles. Here, we demonstrate that plant cell walls are determinants of immune responses since modification of their composition in a set ofArabidopsiscell wall mutants has an impact on their disease resistance and fitness phenotypes. In these genotypes, we identified specific correlations between the amounts of specific wall carbohydrate epitopes and disease resistance/fitness phenotypes through mathematical analyses. These data support the relevant and specific function of plant cell wall composition in plant immune responses and provide the basis for using wall traits in crop breeding programs.

Summary: Fungal cell walls, which are essential for environmental adaptation and host colonization by the fungus, have been evolutionarily selected by plants and animals as a source of microbe‐associated molecular patterns (MAMPs) that, upon recognition by host pattern recognition receptors (PRRs), trigger immune responses conferring disease resistance. Chito‐oligosaccharides [β‐1,4‐N‐acetylglucosamine oligomers, (GlcNAc)_n] are the only glycosidic structures from fungal walls that have been well‐demonstrated to function as MAMPs in plants. Perception of (GlcNAc)_4–8 by Arabidopsis involves CERK1, LYK4 and LYK5, three of the eight members of the LysM PRR family. We found that a glucan‐enriched wall fraction from the pathogenic fungus Plectosphaerella cucumerina which was devoid of GlcNAc activated immune responses in Arabidopsis wild‐type plants but not in the cerk1 mutant. Using this differential response, we identified the non‐branched 1,3‐β‐d‐(Glc) hexasaccharide as a major fungal MAMP. Recognition of 1,3‐β‐d‐(Glc)₆ was impaired in cerk1 but not in mutants defective in either each of the LysM PRR family members or in the PRR‐co‐receptor BAK1. Transcriptomic analyses of Arabidopsis plants treated with 1,3‐β‐d‐(Glc)₆ further demonstrated that this fungal MAMP triggers the expression of immunity‐associated genes. In silico docking analyses with molecular mechanics and solvation energy calculations corroborated that CERK1 can bind 1,3‐β‐d‐(Glc)₆ at effective concentrations similar to those of (GlcNAc)₄. These data support that plants, like animals, have selected as MAMPs the linear 1,3‐β‐d‐glucans present in the walls of fungi and oomycetes. Our data also suggest that CERK1 functions as an immune co‐receptor for linear 1,3‐β‐d‐glucans in a similar way to its proposed function in the recognition of fungal chito‐oligosaccharides and bacterial peptidoglycan MAMPs.

Summary: Pattern‐triggered immunity (PTI) is activated in plants upon recognition by pattern recognition receptors (PRRs) of damage‐ and microbe‐associated molecular patterns (DAMPs and MAMPs) derived from plants or microorganisms, respectively. To understand better the plant mechanisms involved in the perception of carbohydrate‐based structures recognized as DAMPs/MAMPs, we have studied the ability of mixed‐linked β‐1,3/1,4‐glucans (MLGs), present in some plant and microbial cell walls, to trigger immune responses and disease resistance in plants. A range of MLG structures were tested for their capacity to induce PTI hallmarks, such as cytoplasmic Ca²⁺ elevations, reactive oxygen species production, phosphorylation of mitogen‐activated protein kinases and gene transcriptional reprogramming. These analyses revealed that MLG oligosaccharides are perceived by Arabidopsis thaliana and identified a trisaccharide, β‐d‐cellobiosyl‐(1,3)‐β‐d‐glucose (MLG43), as the smallest MLG structure triggering strong PTI responses. These MLG43‐mediated PTI responses are partially dependent on LysM PRRs CERK1, LYK4 and LYK5, as they were weaker in cerk1 and lyk4 lyk5 mutants than in wild‐type plants. Cross‐elicitation experiments between MLG43 and the carbohydrate MAMP chitohexaose [β‐1,4‐d‐(GlcNAc)₆], which is also perceived by these LysM PRRs, indicated that the mechanism of MLG43 recognition could differ from that of chitohexaose, which is fully impaired in cerk1 and lyk4 lyk5 plants. MLG43 treatment confers enhanced disease resistance in A. thaliana to the oomycete Hyaloperonospora arabidopsidis and in tomato and pepper to different bacterial and fungal pathogens. Our data support the classification of MLGs as a group of carbohydrate‐based molecular patterns that are perceived by plants and trigger immune responses and disease resistance.

Plant cells can be distinguished from animal cells by their cell walls and high-turgor pressure. Although changes in turgor and the stiffness of cell walls seem coordinated, we know little about the mechanism responsible for coordination. Evidence has accumulated that plants, like yeast, have a dedicated cell wall integrity maintenance mechanism. It monitors the functional integrity of the wall and maintains integrity through adaptive responses induced by cell wall damage arising during growth, development, and interactions with the environment. These adaptive responses include osmosensitive induction of phytohormone production, defense responses, as well as changes in cell wall composition and structure. Here, we investigate how the cell wall integrity maintenance mechanism coordinates changes in cell wall stiffness and turgor in Arabidopsis thaliana. We show that the production of abscisic acid (ABA), the phytohormone-modulating turgor pressure, and responses to drought depend on the presence of a functional cell wall. We find that the cell wall integrity sensor THESEUS1 modulates mechanical properties of walls, turgor loss point, ABA biosynthesis, and ABA-controlled processes. We identify RECEPTOR-LIKE PROTEIN 12 as a component of cell wall integrity maintenance–controlling, cell wall damage–induced jasmonic acid (JA) production. We propose that THE1 is responsible for coordinating changes in turgor pressure and cell wall stiffness. Significance Plants need to constantly adapt to a changing environment. Adaptation includes responses to biotic and abiotic stress. Key elements determining the response to abiotic stress are the cell walls surrounding all plant cells and the phytohormone abscisic acid, which influence turgor pressure in plants. Turgor pressure in plant cells is much higher than in animal cells and a key driver of plant growth and development. Here, we investigate the mechanism regulating cell wall stiffness and coordinating changes in stiffness and turgor with abscisic acid production. We characterize key elements of the mechanism and dissect its mode of action. This knowledge will enable us to improve plant resistance to drought stress, which is necessary due to our changing environment.