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. 2008 Aug;20(8):2009-17.
doi: 10.1105/tpc.108.060194. Epub 2008 Aug 22.

From Guard to Decoy: a new model for perception of plant pathogen effectors

Renier A L van der Hoorn  1 , Sophien Kamoun
Affiliations

From Guard to Decoy: a new model for perception of plant pathogen effectors

Renier A L van der Hoorn et al. Plant Cell. 2008 Aug.

Abstract

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.

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Figures

Figure 1.
Figure 1.
Opposing Selection Forces on Guarded Effector Targets in a Plant Population Polymorphic for R Genes. Opposing selection forces are expected to operate on guarded effector targets in plants with or without the associated R protein. In the absence of the R protein (green arrows), targets will be under selective pressure to reduce the interaction and evade manipulation (left). In the presence of the R protein (red arrows), the guarded effector target will be under selective pressure to improve the interaction with the effector and enhance pathogen perception (right). The figure represents protein complexes, but similar models can be drawn for nonprotein effector targets. A gene duplication of the effector target or the independent evolution of a target mimic would reduce the evolutionary constraints imposed on the guarded effector target, allowing it to specialize as a coreceptor (decoy) that regulates the activation of the R protein.
Figure 2.
Figure 2.
Comparisons of the Guard and Decoy Models. The classical Guard Model (A) is contrasted with a modified Guard Model in which the effector targets multiple plant proteins (B) and the Decoy Model (C). Effectors are depicted in gray, operative effector targets in purple, guardee in green, decoy in blue, and the R protein in orange.
Figure 3.
Figure 3.
Genetic Tests to Discriminate between the Guard and Decoy Models. Plants lacking both the R protein and the presumed operative target(s) should be challenged with pathogens in the absence or presence of the guardee/decoy. A differential pathogen growth supports the Guard Model, whereas an unaffected pathogen growth supports the Decoy Model. The test of choice depends on the nature of the effector. (A) Effectors that promote positive effects on pathogen growth by manipulating their target should be present during the test to reveal target contributions. (B) Effectors that prevent negative effects on pathogen growth should be omitted to avoid them from suppressing a possible phenotype.
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References

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