ABSTRACT
Immunity in the plant kingdom mainly relies on the pattern-triggered immunity (PTI) and the effector-triggered immunity (ETI). PTI is activated by microbe-associated molecular patterns (MAMPs), whereas ETI is activated by genotype-specific effectors released by microbes into the plant cell to enhance pathogenicity. The multitude of MAMPs, pathogenicity effectors and corresponding plant receptors derive from the long co-evolutionary arms race between plants and pathogens. However, the first line of defence against invading pathogens is typically the plant cell wall and is the first battleground for survival. The degradation of the plant cell wall by microbial cell wall degrading enzymes (CWDEs) is opposed by plant-encoded CWDE inhibitors. Moreover, several damage-associated molecular patterns (DAMPs) are key molecular indicators of cell wall damage and derive from its degradation. The necessity to repair and defend mechanical wounds to prevent them from being an easy passageway for microbes into plant cells and tissues appears to have been a key factor in the evolution of plant immunity. Cell wall–derived DAMPs trigger a PTI-like response and share early transduction events and many downstream responses with MAMPs. It is conceivable that MAMPs evolved to exploit the mechanisms and pathways of DAMP-mediated defence responses. Synergy between DAMPs and MAMPs may be the key to the activation of a stronger and more efficient plant immune response. The purpose of this book chapter is to provide a historical view of how research on plant cell wall degradation has paved the way to our current understanding of cell wall involvement in immunity.
