Pathogen-Induced Cell Wall Remodeling and Immune Signaling in Plants

Abstract

The plant cell wall is a primary barrier to pathogen invasion and a dynamic extracellular interface involved in defense signaling. During infection, pathogens remodel the wall through cell wall-degrading enzymes and effectors, whereas plants reinforce the wall and perceive wall-derived damage-associated molecular patterns that activate immune responses. Recent studies have refined this view by challenging a simple wall-associated kinase-centered model of oligogalacturonide perception, linking MIK2-associated peptide-receptor pathways to pattern-triggered immunity, and showing that pathogens can chemically modify wall-derived fragments to alter their elicitor activity. In addition to chemical cues, pathogen-induced wall perturbation can also affect physical properties such as wall stiffness, porosity, membrane tension, and localized deformation, although how these inputs are integrated during infection remains incompletely understood. This review summarizes current understanding of pathogen-induced cell wall remodeling, wall-derived immune signaling, receptor-associated wall integrity pathways, and their implications for crop disease resistance. We highlight emerging connections among wall chemistry, wall mechanics, peptide signaling, hormone regulation, and growth–defense trade-offs as important directions for understanding wall-mediated immunity.

Plant diseases continue to threaten agricultural productivity and the stability of natural and managed ecosystems. Pathogen entry and colonization often begin at the host surface, where the cell wall and apoplast form the first extracellular environment encountered by invading microbes. The plant cell wall is composed mainly of cellulose, hemicelluloses, pectins, structural proteins, and phenolic polymers, and it provides mechanical support while restricting pathogen access. However, this barrier-centered view is incomplete because the wall also participates in the detection and transmission of pathogen-induced damage signals (Bacete et al., 2018; Molina et al., 2024; Munzert and Engelsdorf, 2025).

During infection, the cell wall is actively remodeled by both pathogen and host activities. Pathogen-derived enzymes and effectors weaken wall structure, promote tissue colonization, and alter the apoplastic environment, whereas plants reinforce and remodel the wall through localized deposition of defense-related materials, modification of wall polymers, and secretion of defense proteins. These processes can generate wall-derived fragments and alter wall properties, thereby linking structural damage to receptor-associated immune signaling (Bacete et al., 2018; Molina et al., 2024; Vaahtera et al., 2019). Plants detect extracellular danger signals through cell-surface receptors. Damage-associated molecular patterns (DAMPs) are host-derived molecules or fragments that become immune-active after tissue damage, cell wall degradation, or abnormal extracellular release. By contrast, microbe-associated molecular patterns (MAMPs) are conserved microbial molecules, such as bacterial flagellin, elongation factor Tu, or fungal chitin, that are perceived as non-self signals. Recognition of DAMPs or MAMPs by pattern-recognition receptors (PRRs) activates pattern-triggered immunity (PTI), an early layer of inducible defense that includes Ca²⁺ influx, reactive oxygen species (ROS) production, mitogen-activated protein kinase (MAPK) activation, defense gene expression, and local wall reinforcement. Cell wall integrity (CWI) signaling refers more broadly to cellular responses associated with altered wall composition, structure, or physical status (Bacete et al., 2018; Gronnier et al., 2022; Yang et al., 2021).

A central question is how plants interpret wall perturbation during infection. Chemical information is provided by wall-derived fragments, including oligogalacturonides (OGs) and cellulose-derived cellodextrins (CDs), as well as microbial glycans released into the apoplast. In parallel, physical changes such as altered wall stiffness, porosity, membrane tension, turgor-related imbalance, and local deformation may also influence defense signaling. These chemical and physical inputs are likely integrated through receptor-like kinases, CWI-associated pathways, peptide signaling modules, and mechanosensitive components, but the relative contribution of each layer remains incompletely understood.

The outcome of wall perturbation is highly context-dependent. It varies with pathogen lifestyle, infection stage, tissue type, wall chemistry, and the mechanical state of the extracellular matrix. Wall-associated signaling can overlap with PTI, influence hormone networks, and regulate localized callose deposition and secretion of antimicrobial proteins and wall-modifying enzymes. These responses also create growth–defense trade-offs because reinforcement and repair must be coordinated with normal cell expansion, development, and crop productivity.

Much of the mechanistic evidence discussed in this review comes from Arabidopsis and other plants with pectin-rich Type I primary walls. Therefore, pectin-derived OG signaling, pectin methylesterification, and polygalacturonase (PG)–polygalacturonase-inhibiting protein (PGIP) interactions are treated here as well-characterized examples from pectin-rich systems rather than as universal mechanisms across all plant lineages. This distinction is especially important for Poaceae, which possess Type II primary walls with lower pectin abundance and greater contributions from glucuronoarabinoxylans and mixed-linkage glucans (Carpita and Gibeaut, 1993; Little et al., 2018; Munzert and Engelsdorf, 2025).

This review examines pathogen-induced wall remodeling as an extracellular defense interface. We discuss how pathogens modify the host wall, how plants generate and perceive wall-derived signals, and how receptor-associated pathways, wall mechanics, hormone regulation, and crop-level constraints shape wall-mediated disease resistance.

The Plant Cell Wall as a Defense-Related Extracellular Interface

Wall-mediated defense is shaped by the physical and chemical properties of the extracellular matrix. Cellulose, hemicelluloses, pectins, structural proteins, phenolic polymers, and apoplastic enzymes together determine wall strength, flexibility, enzyme accessibility, and the production of defense-related fragments during infection. These properties influence multiple stages of plant–pathogen interactions, including pathogen penetration, tissue maceration, apoplastic colonization, wall-derived signal release, and downstream defense activation (Dora et al., 2022; Molina et al., 2024; Munzert and Engelsdorf, 2025).

The contribution of wall properties to disease resistance depends strongly on tissue type, developmental stage, pathogen lifestyle, and infection phase. Leaves, roots, vascular tissues, fruits, and reproductive organs differ in wall composition, pectin chemistry, lignification, cuticle association, and apoplastic conditions. Therefore, a wall trait that restricts pathogen entry in one tissue or pathosystem may not provide similar protection in another (Anderson and Kieber, 2020; Molina et al., 2024; Munzert and Engelsdorf, 2025).

Wall-mediated defense therefore does not operate as a single linear pathway. Resistance cannot be inferred from wall thickness, stiffness, or composition alone, but depends on how these features influence pathogen access, enzymatic degradation, release of wall-derived signals, and immune activation within a specific tissue and infection context (De Lorenzo and Cervone, 2022; Molina et al., 2024; Vaahtera et al., 2019).

Pathogen Strategies for Remodeling the Host Cell Wall

Pathogens remodel the host cell wall to promote infection. Fungal and bacterial pathogens secrete cell wall-degrading enzymes (CWDEs) that target pectin, cellulose, hemicelluloses, and associated wall polymers, thereby weakening host tissues, releasing nutrients, and facilitating apoplastic colonization (Kubicek et al., 2014). Necrotrophic fungi such as Botrytis cinerea and Sclerotinia sclerotiorum, together with soft-rot bacteria including Pectobacterium and Dickeya species, rely extensively on degradation of pectin-rich primary walls and the middle lamella to promote tissue maceration and disease development (Charkowski, 2018; Davidsson et al., 2013; Hugouvieux-Cotte-Pattat et al., 2014; Wei et al., 2022). These activities have consequences beyond tissue collapse because the fragments generated during degradation can also influence host signaling.

The extent and timing of wall remodeling differ among pathogen lifestyles. Necrotrophs generally benefit from extensive wall degradation and host cell death, whereas biotrophic pathogens, including rusts and powdery mildews, maintain living host cells and often induce more localized wall modification (Mapuranga et al., 2022; Mendgen and Hahn, 2002). Hemibiotrophic pathogens may limit wall-damaging activity during early colonization and increase CWDE production during the transition to necrotrophy (Kubicek et al., 2014; Munzert and Engelsdorf, 2025; O’Connell et al., 2012). Accordingly, pathogen-induced wall remodeling is best interpreted in relation to infection phase, tissue entry route, and host wall properties.

Secreted effectors may suppress vesicle-mediated delivery of defense-related cargo, including callose synthases, antimicrobial proteins, phenolic compounds, and wall-modifying enzymes, to infection sites. They may also inhibit local wall reinforcement, alter wall-modifying enzyme activity, or disrupt inhibitor–enzyme interactions in the apoplast (Munzert and Engelsdorf, 2025). The apoplastic environment therefore reflects interactions among pathogen enzymes, host inhibitors, oxidative enzymes, antimicrobial proteins, and wall-derived defense signals. These processes influence not only host penetration but also the composition and activity of extracellular defense responses.

The interaction between pathogen-secreted PG and host PGIP provides a clear example of how plants regulate pathogen-mediated pectin degradation. In Arabidopsis, antisense suppression of AtPGIP1 reduced inducible PG-inhibiting activity and increased susceptibility to B. cinerea, supporting a role for PGIP activity in basal resistance to a pectin-degrading necrotroph (Ferrari et al., 2006). Conversely, S. sclerotiorum secretes the extracellular effector SsPINE1, which interacts with host PGIPs, promotes dissociation of PGIP–PG complexes, enhances pectin degradation, and increases fungal virulence. Deletion of SsPINE1 reduced virulence, whereas expression of SsPINE1 in plants decreased resistance, demonstrating that pathogens can overcome host regulation of pectin degradation by targeting PGIP-mediated inhibition (Wei et al., 2022).

Pectin Remodeling as a Central Component of Wall-Mediated Immunity

Pectin-centered mechanisms are best characterized in Arabidopsis and other plants with pectin-rich Type I primary walls. Pectin is abundant in primary walls and the middle lamella and is readily targeted by microbial PGs and pectate lyases (PLs). These enzymes degrade homogalacturonan, promoting tissue loosening and pathogen spread, while partial degradation can generate OGs, thereby linking pectin cleavage to wall-derived immune signaling (De Lorenzo and Cervone, 2022; Degli Esposti et al., 2025; Ferrari et al., 2013).

Pectin methylesterases (PMEs) and pectin methylesterase inhibitors (PMEIs) regulate the degree and pattern of homogalacturonan de-methylesterification. These changes affect wall porosity, calcium cross-linking, stiffness, enzyme accessibility, and susceptibility to pathogen-derived PGs and PLs (Lionetti et al., 2012; Wang et al., 2023). Pectin methylesterification therefore links wall architecture with the pattern of pathogen-mediated cleavage and the likelihood that immune-active fragments will be generated.

PGIPs provide an additional level of control by restricting pathogen PG activity and limiting extensive homogalacturonan degradation. This can favor the accumulation of elicitor-active OGs rather than complete pectin digestion (Ferrari et al., 2013). Together, pectin methylesterification and PGIP-mediated regulation influence whether pectin remodeling primarily supports pathogen colonization or contributes to defense signaling. The outcome is shaped by host enzymes, pathogen enzymes, wall chemistry, and apoplastic conditions rather than by a single pectin modification (Fig. 1).

Fig. 1.

Pectin-centered remodeling of the plant cell wall during pathogen infection. (A) Pathogen-derived PGs and PLs cleave HG in pectin-rich wall regions, promoting wall loosening, increased porosity, and OG generation. (B) PMEs and PMEIs regulate pectin methylesterification, thereby influencing Ca²⁺ cross-linking, wall stiffness, enzyme accessibility, and fragment production. (C) Pathogen-derived GOXs can reduce OG elicitor activity, whereas PGIPs restrict pathogen PG activity and favor the accumulation of elicitor-active OGs. Thus, pectin remodeling links wall architecture, enzyme accessibility, OG production, and wall-mediated immunity. GalA, galacturonic acid; HG, homogalacturonan; Me, methyl ester; PME, pectin methylesterase; PMEI, pectin methylesterase inhibitor; PGs, polygalacturonases; PLs, pectate lyases; OGs, oligogalacturonides; PGIPs, polygalacturonase-inhibiting proteins; GOXs, galacturonide oxidases.

Wall-Derived DAMPs and Oligosaccharide Elicitors

Wall-derived DAMPs provide a mechanism by which plants detect pathogen-associated wall damage. OGs are the best-characterized wall-derived DAMPs and are associated with ROS production, MAPK activation, defense gene expression, callose deposition, and enhanced resistance. Their activity depends on structural features such as degree of polymerization, methylesterification or oxidation state, and persistence in the apoplast. Experimental release of OGs in planta and treatment with cellulose-derived CDs further support the idea that wall fragments can function as immune-active signals rather than only as structural breakdown products (Benedetti et al., 2015; De Lorenzo and Cervone, 2022; Degli Esposti et al., 2025; Souza et al., 2017).

Extracellular oligosaccharide elicitors are not limited to OGs. CDs derived from cellulose and oligosaccharides released from hemicelluloses have also been associated with defense activation, indicating that several plant wall polymers can generate immune-active fragments under appropriate conditions (Souza et al., 2017; Sun et al., 2025). Microbial cell wall-derived glycans, including chitin- and glucan-related fragments, can also act as extracellular elicitors when perceived by plant receptor systems (Sun et al., 2025). Plant wall-derived fragments are generally classified as DAMPs, whereas microbial wall-derived glycans are more appropriately considered microbe-associated elicitors.

In grasses, wall-derived immune signaling may involve polymers that differ from the pectin-rich systems characterized in Arabidopsis. In rice, the blast fungus Magnaporthe oryzae secretes two endoglucanases, MoCel12A and MoCel12B, which release Poaceae-associated oligosaccharides from rice hemicellulose. These oligosaccharides activate OsCERK1/OsCEBiP-dependent immune responses, including ROS production, MAPK activation, defense gene expression, and enhanced resistance to rice blast (Yang et al., 2021). This example indicates that wall-derived oligosaccharide signaling also operates in cereals, but the relevant wall polymers and receptor systems can differ from pectin-centered dicot models.

Several questions remain unresolved, including which fragments are generated during natural infection, how long they persist, how they are chemically modified, and which receptor systems perceive them. Infection-stage-specific apoplast profiling, structural glycomics, and receptor genetics may help define how wall-derived DAMPs contribute to resistance across different plant–pathogen systems.

Receptor systems linking wall perturbation to immune signaling

Pathogen-induced wall perturbation can be connected to immune signaling through several types of cell-surface components. These include receptor-associated pathways linked to wall-derived fragments, peptide-mediated modules associated with wall integrity or immune regulation, and mechanosensitive channels that may convert physical perturbation into ion fluxes. These pathways are not equivalent to one another. Some recognize extracellular ligands directly, whereas others regulate immune receptor complex formation or respond to altered wall status.

Several components discussed in this section overlap with PTI. FLS2 and EFR are bacterial PRRs that perceive flagellin-derived and elongation factor Tu-derived peptides, respectively. BAK1/SERK3 is a shared co-receptor recruited by several activated PRR complexes, including FLS2 and EFR. These complexes activate typical early immune outputs, including Ca²⁺ influx, ROS production, MAPK signaling, and defense gene expression (Bacete et al., 2018; De Lorenzo and Cervone, 2022; Molina et al., 2024).

Wall-associated kinases (WAKs) were initially proposed as receptors for OGs, pectin-derived DAMPs released during pathogen-mediated wall degradation (Brutus et al., 2010). A chimeric receptor containing the WAK1 extracellular domain and the EFR intracellular kinase domain supported this idea, as it mediated OG-responsive signaling (Brutus et al., 2010). However, an Arabidopsis wak1–wak5 mutant retains OG-induced early signaling, transcriptional responses, and resistance to bacterial and fungal pathogens, indicating that WAK1–WAK5 are dispensable for OG-induced immunity and that the receptor responsible for direct OG perception remains unresolved (Herold et al., 2025). WAKs may nevertheless contribute to pectin-associated signaling or wall status control independently of primary OG recognition (Brutus et al., 2010; Herold et al., 2025).

Beyond wall-derived carbohydrate fragments, wall perturbation can also intersect with peptide-mediated signaling at the cell surface. The SCOOP–MIK2 and RALF–FER pathways illustrate two routes that connect altered wall status, plasma membrane receptor organization, and PTI, while remaining distinct from direct wall-derived DAMP perception.

The SCOOP–MIK2 pathway links altered wall status to immune signaling through secreted peptide ligands. SCOOPs are serine-rich endogenous peptides and are therefore distinct from carbohydrate fragments released during wall degradation. MIK2 perceives SCOOP ligands and recruits the co-receptors BAK1/SERK3 or SERK4, leading to Ca²⁺ influx, apoplastic ROS production, MAPK signaling, defense-related transcription, and growth inhibition (Hou et al., 2021; Rhodes et al., 2021). Structural analyses further show that the conserved SxS motif of SCOOP peptides mediates binding to MIK2, whereas C-terminal residues stabilize association with BAK1, supporting ligand-dependent assembly of an active MIK2–BAK1 receptor complex (Wu et al., 2024).

The connection between MIK2 and wall remodeling is supported by experiments in which cellulose biosynthesis was inhibited to alter wall integrity. Under these conditions, PROSCOOP18 expression is induced, and the SCOOP18–MIK2 module contributes to lignification and potentiation of PTI (Zhai et al., 2024). This finding suggests that altered wall status can promote peptide-mediated immune signaling. However, MIK2 has not been shown to directly recognize damaged cellulose, wall-derived carbohydrate fragments, or a defined mechanical change. Although PROSCOOP18 expression is also induced after infection with Pseudomonas syringae pv. tomato DC3000 and Botrytis cinerea, the processing, secretion, and activity of endogenous SCOOP18 during natural infection remain incompletely understood (Zhai et al., 2024). MIK2 can also perceive SCOOP-like peptides from Fusarium proteins, indicating that it responds to both endogenous phytocytokines and structurally related microbial peptides (Hou et al., 2021; Rhodes et al., 2021).

RALF–FER signaling provides a separate route through which peptide signaling can influence cell-surface immune responses. FERONIA (FER), a member of the Catharanthus roseus receptor-like kinase 1-like (CrRLK1L) family, acts as a regulatory scaffold at the plasma membrane. In the absence of inhibitory Rapid Alkalinization Factor 23 (RALF23) signaling, FER supports ligand-induced association of the bacterial PRRs FLS2 and EFR with the shared co-receptor BAK1, promoting PRR complex formation and downstream PTI signaling (Stegmann et al., 2017). By contrast, mature RALF23 is perceived by an extracellular LLG–FER complex. LORELEI-like glycosylphosphatidylinositol (GPI)-anchored proteins (LLGs), particularly LLG1, bind RALF23 and support formation of RALF23–LLG–FER complexes, which reduce FLS2–BAK1 and EFR–BAK1 association and attenuate PTI (Gronnier et al., 2022; Stegmann et al., 2017; Xiao et al., 2019).

The relevance of RALF–FER signaling to wall-mediated immunity lies in its role in organizing receptor complexes at the cell surface and integrating peptide signaling with growth and defense. Pathogen- or parasite-derived RALF-like peptides can exploit related receptor pathways, but FER has not been shown to directly perceive defined wall fragments or physical wall damage during infection. RALF–FER signaling can therefore be viewed as a peptide-regulated immune-modulatory pathway that intersects with wall-associated signaling and PTI, rather than as a direct DAMP receptor pathway (Gronnier et al., 2022; Stegmann et al., 2017; Tang et al., 2022; Xiao et al., 2019).

THESEUS1 (THE1), another member of the CrRLK1L family, represents a CWI-linked branch of this receptor family. THE1 was identified through its role in responses to cellulose biosynthesis defects and contributes to growth inhibition, ectopic lignification, and stress-associated transcription after wall disruption (Gonneau et al., 2018; Hématy et al., 2007). RALF34 binds the THE1 extracellular domain and induces THE1-dependent apoplastic alkalinization, mainly in root tissues (Gonneau et al., 2018). However, it is not yet clear whether RALF34 is the relevant ligand during pathogen-induced wall damage, and direct recognition of pathogen-derived molecules or defined wall fragments by THE1 has not been demonstrated (Gonneau et al., 2018; Zwartkruis et al., 2026). THE1 is therefore best regarded as a receptor that monitors wall integrity and contributes to defense-associated responses, even though the molecular steps linking pathogen-mediated wall degradation to its activation remain unresolved (Gonneau et al., 2018; Hématy et al., 2007; Zwartkruis et al., 2026).

Physical changes associated with pathogen penetration, such as local deformation, altered wall stiffness, membrane tension, cell swelling, and turgor-related changes, may provide additional inputs into these responses. Mechanosensitive channels including PIEZO, OSCA/TMEM63, and MscS-like (MSL) proteins offer potential routes for converting mechanical perturbation into ion fluxes (Hamilton et al., 2015; Murthy et al., 2018; Moussavi et al., 2021). In plant immunity, OSCA1.3 has been linked to immune-associated stomatal closure, and Arabidopsis MSL10 provides a relevant example connecting mechanosensitive channels with bacterial pathogen responses (Thor et al., 2020). MSL10 hypermorphic alleles show ROS accumulation, spontaneous cell death, and reduced susceptibility to Pseudomonas syringae pv. tomato DC3000 and avirulent strains carrying avrRpt2 or avrRpm1, whereas the msl10-1 mutant shows delayed pathogenesis-related 1 (PR1) induction, reduced stomatal closure, and modestly increased susceptibility to coronatine-deficient P. syringae. These findings suggest that MSL10 can modulate pathogen responses and may connect membrane or wall-associated mechanical perturbation with Ca²⁺/ROS-dependent immune outputs (Basu et al., 2022). However, whether MSL10 directly senses pathogen-induced wall remodeling remains unresolved. Thus, MSL10 and related mechanosensitive channels are best viewed as plausible contributors to mechanically coupled immune signaling rather than canonical pathogen receptors (Fig. 2).

Fig. 2.

Receptor-associated pathways linking wall perturbation to immune signaling. (A) Wall-derived fragments, altered wall integrity, peptide ligands, and physical perturbation can engage distinct plasma membrane-associated pathways. WAKs are linked to pectin-associated signaling, although direct OG perception remains unresolved. (B) The SCOOP–MIK2 module connects altered wall status with peptide-mediated PTI potentiation. (C) FER–LLG supports FLS2/EFR–BAK1 complex formation in the RALF23-free state, whereas mature RALF23 binding to the extracellular LLG–FER complex reduces these associations and attenuates PTI. (D) THE1 is shown with an unresolved altered-wall-integrity input, and mechanosensitive channels are shown as possible contributors to ion fluxes and mechanically coupled immune outputs. These pathways converge on Ca²⁺ influx, ROS production, MAPK activation, defense gene expression, callose deposition, lignification, and secretion of antimicrobial or wall-reinforcing proteins. MIK2, MDIS1-Interacting Receptor Like Kinase 2; BAK1, BRI1-Associated Receptor Kinase 1; SERK4, Somatic Embryogenesis Receptor Kinase 4; FER, FERONIA; LLG1, LORELEI-Like GPI-Anchored Protein 1; FLS2, FLAGELLIN-SENSING 2; EFR, EF-TU RECEPTOR; WAKs, Wall-Associated Kinases; THE1, THESEUS1; RLCK, Receptor-Like Cytoplasmic Kinase; BIK1, BOTRYTIS-INDUCED KINASE 1; PBL, PBS1-LIKE; SCOOP, Serine-rich Endogenous Peptide; PROSCOOP, PRO-Serine-rich Endogenous Peptide; RALF, Rapid Alkalinization Factor; flg22, 22-amino-acid flagellin epitope; elf18, 18-amino-acid elongation factor Tu epitope.

Together, these pathways outline multiple routes by which pathogen-induced wall perturbation can reach the immune network. Pectin degradation generates OGs, whose direct receptor remains unknown; experimentally induced wall perturbation can induce PROSCOOP18 expression and activate SCOOP18–MIK2 signaling; microbial SCOOP-like peptides may also engage MIK2; RALF–FER signaling modulates PRR complex formation; THE1 contributes to CWI-associated responses; and mechanosensitive channels may connect physical perturbation with ion fluxes and immune outputs (Basu et al., 2022; Brutus et al., 2010; Gonneau et al., 2018; Hématy et al., 2007; Hou et al., 2021; Rhodes et al., 2021; Stegmann et al., 2017; Thor et al., 2020; Zhai et al., 2024). These pathways converge with PTI at the level of Ca²⁺ signaling, ROS production, MAPK activation, defense gene expression, lignification, callose deposition, and secretion of antimicrobial or wall-reinforcing proteins (Bacete et al., 2018; De Lorenzo and Cervone, 2022; Molina et al., 2024).

Wall Reinforcement and Hormonal Regulation

Callose deposition is a major component of local, wall-associated defense. Callose accumulates at papillae, plasmodesmata, and sites of attempted penetration, where it can limit pathogen entry, hyphal growth, or intercellular spread. Its protective effect depends on when and where it is deposited and on pathogen lifestyle. In Arabidopsis, overexpression of the callose synthase PMR4/GSL5 enhances early callose accumulation at powdery mildew penetration sites and increases penetration resistance, whereas pmr4/gsl5 mutants show variable disease phenotypes in different pathosystems (Bacete et al., 2018; Ellinger et al., 2013; Molina et al., 2024). Callose therefore functions most effectively as a rapid and localized barrier rather than as a uniformly protective wall modification.

Lignification and oxidative cross-linking provide additional reinforcement at infection sites. Pathogen challenge can stimulate peroxidase-dependent coupling of phenolic compounds, lignin deposition, and strengthening of the wall around penetration sites or infected tissues. These changes can reduce wall digestibility, limit pathogen access to the apoplast, and restrict lesion expansion or vascular colonization, but extensive or long-lasting lignification may interfere with cell expansion, transport, and normal tissue function. Lignin- and phenolic-based reinforcement is therefore most effective when confined to sites of pathogen ingress or spread rather than induced constitutively throughout the plant (Bacete et al., 2018; Molina et al., 2024).

Hormonal regulation shapes the strength and composition of these wall responses. SA-linked signaling is often associated with resistance to biotrophic and some hemibiotrophic pathogens, whereas JA and ET more commonly contribute to defense against necrotrophs. These pathways regulate callose synthases, peroxidases, phenylpropanoid enzymes, pectin-modifying proteins, and secreted antimicrobial proteins, while wall-derived fragments and apoplastic changes can feed back on hormone signaling. Thus, wall remodeling and hormone pathways form a reciprocal regulatory network whose outcome depends on pathogen lifestyle, infection stage, and tissue context (Bacete et al., 2018; De Lorenzo and Cervone, 2022).

Pathogen manipulation of wall-derived signals and crop applications

Pathogens can influence wall-derived immune signaling not only by controlling the release of DAMPs but also by changing their chemical state after they are produced. Secreted berberine bridge enzyme-like galacturonide oxidases from Phytophthora infestans illustrate this principle. These enzymes are induced early during infection and oxidize the reducing ends of pectin-derived OGs. Longer oxidized OGs show reduced ability to trigger ROS production in Arabidopsis and tomato, and silencing of the corresponding pathogen genes reduces infection success (Welsh et al., 2025). These observations indicate that chemical modification of wall-derived DAMPs can act as a virulence mechanism by lowering their immunogenicity before host receptors can perceive them (Welsh et al., 2025).

The outcome of wall degradation is therefore determined not only by how much wall is broken down or which fragment sizes are released, but also by subsequent oxidation, hydrolysis, sequestration, or further degradation of fragments in the apoplast. Pathogens can shape the wall-derived signal pool at multiple steps, including fragment production, chemical modification, stability, and access to host receptors. This perspective helps explain why structurally related wall fragments can differ in immune activity among pathosystems and why extensive wall degradation does not always lead to proportionally strong DAMP signaling.

The effects of wall remodeling are strongly shaped by tissue, infection site, and cell type. Cell wall composition differs among species, organs, developmental stages, and cell populations, and pathogens encounter distinct structural and chemical conditions in epidermal, mesophyll, root, vascular, fruit, and reproductive tissues. Foliar pathogens may penetrate epidermal walls or enter through stomata, whereas root and vascular pathogens often exploit wounds, lateral root emergence sites, or developmentally weak interfaces. Because infection-associated wall remodeling is often restricted to pathogen contact sites or specific cell populations, whole-organ measurements may obscure local changes in pectin status, arabinogalactan protein abundance, callose deposition, or lignification. Single-cell and spatial approaches can help distinguish wall changes caused directly by pathogen enzymes from those induced by host immune signaling, which is important because the same wall modification may be beneficial in one cell layer but harmful in another (Munzert and Engelsdorf, 2025).

These considerations place important limits on how wall-based resistance can be used in crops. Constitutive alteration of cellulose, pectin, lignin, or wall-associated signaling can increase resistance in some interactions but can also affect cell expansion, vascular function, organ texture, ripening, biomass, or yield (Molina et al., 2024; Munzert and Engelsdorf, 2025). Recent work therefore favors wall traits that strengthen specific infection sites or are activated after challenge, rather than uniformly increasing wall stiffness throughout the plant (Molina et al., 2024; Munzert and Engelsdorf, 2025). For cereals, Type II wall composition is an important consideration for wall-based resistance strategies, because immune-active fragments and relevant wall-modifying enzymes may differ from those characterized in Arabidopsis and other pectin-rich dicot systems (Carpita and Gibeaut, 1993; Little et al., 2018; Munzert and Engelsdorf, 2025).

Wall- and microbe-derived oligosaccharides can enhance plant immunity, but their resistance-enhancing activity depends on the plant species, pathogen, host genotype, and treatment conditions. The β-1,2-glucan trisaccharide B2G3 enhanced resistance to Pseudomonas syringae pv. tomato DC3000 in Arabidopsis and reduced Colletotrichum higginsianum colonization in the hypersusceptible pgm background. However, B2G3 did not reduce Botrytis cinerea disease under the tested conditions. In monocots, B2G3 induced ROS production in maize and wheat and reduced disease caused by Colletotrichum graminicola in maize and Zymoseptoria tritici in wheat (Fuertes-Rabanal et al., 2024). These findings suggest that β-1,2-glucan-induced resistance can extend beyond a single model species, but its outcome depends on host species, pathogen, genetic background, and assay conditions. Translation to field use will also depend on fragment structure, degree of polymerization, chemical stability, formulation, delivery, persistence, crop genotype, developmental stage, and pathogen pressure.

Conclusion

Pathogen-induced cell wall remodeling is best viewed as a dynamic extracellular process in which wall degradation, damage signal production, receptor-associated signaling, and host reinforcement occur within the same apoplastic space. A major unresolved issue is how plants distinguish wall-derived chemical cues from physical changes such as altered stiffness, porosity, membrane tension, and localized deformation during infection.

Several questions remain central. The receptors that directly perceive many wall-derived fragments, including OGs, are still incompletely defined, as illustrated by recent evidence challenging a simple WAK-centered model of OG perception (Brutus et al., 2010; Herold et al., 2025). The relationship between wall-derived DAMPs, peptide–receptor modules such as MIK2–SCOOP, regulatory receptors such as FER and THE1, mechanosensitive channels, and hormone-associated transcriptional programs also requires further clarification (Basu et al., 2022; Gonneau et al., 2018; Stegmann et al., 2017; Zhai et al., 2024; Zhang et al., 2020). These pathways are unlikely to act independently. Instead, they probably converge in a tissue- and infection-stage-specific manner, influencing whether wall remodeling leads to resistance, repair, growth restriction, or susceptibility.

Future progress will require approaches that preserve infection context. Infection-stage-specific apoplast profiling, structural glycomics, receptor genetics, and live-cell imaging of localized wall remodeling can be combined with single-cell and spatial analyses to resolve cell type-specific responses. These approaches may help define which wall fragments are produced during natural infection, how they are chemically modified, how long they persist, and which receptor systems perceive them. For crop application, wall-associated resistance traits will need to be tuned to strengthen vulnerable infection sites without imposing excessive costs on growth, yield, or quality (Molina et al., 2024; Munzert and Engelsdorf, 2025). Comparative studies of Type I and Type II wall systems may help determine how wall composition shapes the production, perception, and immune activity of wall-derived damage signals.

Thus, pathogen-induced wall remodeling can be viewed not only as wall damage or DAMP production, but as an integrated extracellular interface where chemical cues, physical changes, receptor signaling, hormone networks, and growth–defense trade-offs converge.