Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2014 May 6:5:178.
doi: 10.3389/fpls.2014.00178. eCollection 2014.

The role of the cell wall in plant immunity

Frederikke G Malinovsky  1 , Jonatan U Fangel  2 , William G T Willats  2
Affiliations
Review

The role of the cell wall in plant immunity

Frederikke G Malinovsky et al. Front Plant Sci. .

Abstract

The battle between plants and microbes is evolutionarily ancient, highly complex, and often co-dependent. A primary challenge for microbes is to breach the physical barrier of host cell walls whilst avoiding detection by the plant's immune receptors. While some receptors sense conserved microbial features, others monitor physical changes caused by an infection attempt. Detection of microbes leads to activation of appropriate defense responses that then challenge the attack. Plant cell walls are formidable and dynamic barriers. They are constructed primarily of complex carbohydrates joined by numerous distinct connection types, and are subject to extensive post-synthetic modification to suit prevailing local requirements. Multiple changes can be triggered in cell walls in response to microbial attack. Some of these are well described, but many remain obscure. The study of the myriad of subtle processes underlying cell wall modification poses special challenges for plant glycobiology. In this review we describe the major molecular and cellular mechanisms that underlie the roles of cell walls in plant defense against pathogen attack. In so doing, we also highlight some of the challenges inherent in studying these interactions, and briefly describe the analytical potential of molecular probes used in conjunction with carbohydrate microarray technology.

Keywords: DAMP; PAMP; PTI; callose; chitin; defense; immunity; plant cell wall.

PubMed Disclaimer

Figures

FIGURE 1
FIGURE 1
The “arms race” between Cladosporium fulvum and plant hosts. As a general protective measure against fungal infections plants respond to infection attempts by secreting chitinases into the apoplastic space. The tomato leaf mould fungus C. fulvum can enter its host through stomatal openings, and grows as extracellular hyphae. To shield against the action of these chitin-degrading enzymes the fungus camouflages its chitin-containing cell walls by cloaking them with the chitin-binding effector Avr4 (van den Burg et al., 2006; Hadwiger, 2013). The presence of Avr4 can be recognized by the Tomato RLP Cf-4, leading to induction of the hypersensitive response (Thomas et al., 1997; Takken et al., 1999). Chitin oligomers released by chitinases are recognized as PAMPs, in Arabidopsis by the RLK CERK1 (Iizasa et al., 2010; Petutschnig et al., 2010), and in rice by both OsCERK1 and the RLP OsCEBiP (Shimizu et al., 2010). To escape chitin-induced PTI C. fulvum can secrete Ecp6 an effector that functions as a chitin-scavenger removing the chitin oligomers released by the chitinases (de Jonge et al., 2010; Kombrink and Thomma, 2013; Sanchez-Vallet et al., 2013).
FIGURE 2
FIGURE 2
A current model of AtFLS2 signaling. Upon flg22 binding, a complex between FLS2, BIK1, BAK1 (and other SERKs) is formed. Complex formation triggers multiple rapid phosphorylation events resulting in BIK1 release. The signal transduction downstream of ligand perception includes a Ca2+ burst, activation CDPKs and AtRbohD required for the ROS burst, and induction MAPK cascades. Activation of CDPKs and MAPKs is required for full induction of defense genes.
FIGURE 3
FIGURE 3
The plant cell wall. (A) The primary cell wall is constructed of a web of cellulose micro-fibrils, hemicellulose polysaccharides, and the hetero-polysaccharide pectin (Endler and Persson, 2011). (B) Necotrophic pathogens devour their hosts by degrading the plant cell wall, and secreting necrosis-inducing proteins and toxins (Davidsson et al., 2013). The host entry step of such microbes is thought to happen mainly via secretion of cell wall degrading enzymes such as cellulases, pectinases, and hemicellulases (Choquer et al., 2007; Davidsson et al., 2013). Xylanase, degrades the linear backbone of the predominant hemicellulose xylan into xylose residues (Belien et al., 2006; Scheller and Ulvskov, 2010). Pectinases such as polygalacturonases (PGs) and pectate lyases (PLs) degrades the pectic homogalacturonan (HGA) backbone. The HGA in newly synthesized pectin is methyl-esterified, which protects it from degradation by pectinases. De-esterification of HGA by the action of microbial pectin methyl esterases (PMEs) enables access PGs and PLs (Annis and Goodwin, 1997; Wolf et al., 2009; Lionetti et al., 2012). Endo-PGs cleave un-esterified regions while concomitantly releasing the oligogalacturonides (OGAs), oligomeric fragments of the HGA backbone (Annis and Goodwin, 1997; Ferrari et al., 2013). The wall-associated kinases (WAKs) are DAMP sensors that monitor the integrity of pectin by sensing the presence of OGAs (Ferrari et al., 2013). Plants can counter the cocktail of cell wall degrading enzymes by producing proteinaceous inhibitors such as the xylanase inhibitors and PG inhibitor proteins (PGIPs; Belien et al., 2006).
See this image and copyright information in PMC

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

References

    1. Albersheim P., Darvill A., Roberts K., Sederoff R., Staehelin A. (ed.). (2011). Plant Cell Walls. New York, NY: Garland Science, Taylor and Francis Publishing Group, LLC; 52–61
    1. Annis S. L., Goodwin P. H. (1997). Recent advances in the molecular genetics of plant cell wall-degrading enzymes produced by plant pathogenic fungi. Eur. J. Plant Pathol. 103 1–14 10.1023/A:1008656013255 - DOI
    1. Baker L. G., Specht C. A., Lodge J. K. (2011). Cell wall chitosan is necessary for virulence in the opportunistic pathogen Cryptococcus neoformans. Eukaryot. Cell 10 1264–1268 10.1128/Ec.05138-11 - DOI - PMC - PubMed
    1. Beck M., Heard W., Mbengue M., Robatzek S. (2012a). The INs and OUTs of pattern recognition receptors at the cell surface. Curr. Opin. Plant Biol. 15 367–374 10.1016/j.pbi.2012.05.004 - DOI - PubMed
    1. Beck M., Zhou J., Faulkner C., Maclean D., Robatzek S. (2012b). Spatio-temporal cellular dynamics of the Arabidopsis flagellin receptor reveal activation status-dependent endosomal sorting. Plant Cell 24 4205–4219 10.1105/tpc.112.100263 - DOI - PMC - PubMed

LinkOut - more resources