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The Guard Model for disease resistance postulates that plant resistance proteins act by monitoring (guarding) the target of their corresponding pathogen effector. We posit, however, that guarded effector targets are evolutionarily unstable in plant populations polymorphic for resistance (R) genes. Depending on the absence or presence of the R gene, guarded effector targets are subject to opposing selection forces (1) to evade manipulation by effectors (weaker interaction) and (2) to improve perception of effectors (stronger interaction). Duplication of the effector target gene or independent evolution of a target mimic could relax evolutionary constraints and result in a decoy that would be solely involved in effector perception. There is growing support for this Decoy Model from four diverse cases of effector perception involving Pto, Bs3, RCR3, and RIN4. We discuss the differences between the Guard and Decoy Models and their variants, hypothesize how decoys might have evolved, and suggest ways to challenge the Decoy Model.
Plants have evolved sophisticated mechanisms to perceive pathogen attack and trigger an effective innate immune response. An important and well-characterized perception mechanism is based on resistance (R) genes in plants whose products confer recognition of cognate avirulence (Avr) proteins in the pathogen. This gene-for-gene hypothesis was introduced by Flor in the 1940s, and dozens of R-Avr gene combinations have since been characterized (Dangl and Jones, 2001).
Although the gene-for-gene hypothesis isnowfirmly supported by the characterization of many R-Avr gene pairs, the underlying perception mechanism has been subject to debate for more than a decade. Initially it was widely thought that products of R genes act as receptors that directly interact with the products of Avr genes (Keen, 1990). This ligand-receptor model was supported by the fact that some Avr gene products are small and colocalize with R gene products, most of which encode receptor-like proteins carrying Leu-rich repeats (LRRs). Indeed, direct binding of a few R-Avr combinations was found, consistent with a receptor-ligand mode of action (e.g., Jia et al., 2000; Deslandes et al., 2003; Dodds et al., 2006; Ueda et al., 2006). However, for a number of R-Avr combinations, physical interactions have not been observed, and perception is thought to be indirect.
Meanwhile, it has become evident that many Avr proteins contribute to pathogen virulence on plants lacking the...