Bacterial elicitation and evasion of plant innate immunity

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Abstract
An overview of the various mechanisms of bacterial pathogenesis is presented, with a focus on bacterial proteins, protein-secretion systems and small molecules that modulate plant biology. The mechanisms by which plant pathogen recognition receptors (PRRs) recognize bacterial pathogen-associated molecular patterns (PAMPS) are discussed. Latest developments in this field are examined with an emphasis on the flagellin–FLS2 and elongation factor Tu (EF-Tu)–EFR (EF-Tu receptor) systems. PRR-mediated defences represent a significant obstacle for plant pathogens. However, type III effectors that function to suppress PRR-mediated basal defences have been discovered. These effectors have been shown to limit cell wall-based defences and expression of defence-associated genes. Plants probably evolved resistance (R) proteins to recognize the presence of bacterial effectors that suppress PRR-mediated defences. R proteins elicit a strong hypersensitive response that provides immunity to the host plant. Mechanisms of effector–R protein recognition are discussed in the context of current models. In response to plant R proteins, it seems that pathogens have evolved an alternative set of effectors that suppress R-protein-mediated defences. The mechanisms by which effectors suppress R-protein-mediated defences are examined. Current research establishes that resistance to bacterial pathogens is regulated by both PRR- and R-protein-mediated recognition. The outcome of each interaction is dependent on at least four factors: the complement of PAMPS and effectors in the pathogen, and the PRR and R proteins in the host.