From Guard to Decoy: A New Model for Perception of Plant Pathogen Effectors
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. D...
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| Published in | The Plant cell Vol. 20; no. 8; pp. 2009 - 2017 |
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| Main Authors | , |
| Format | Journal Article |
| Language | English |
| Published |
United States
American Society of Plant Biologists
01.08.2008
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| Subjects | |
| Online Access | Get full text |
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| 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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| AbstractList | 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. 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.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. 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. |
| Author | Kamoun, Sophien van der Hoorn, Renier A.L |
| AuthorAffiliation | a Plant Chemetics Lab, Max Planck Institute for Plant Breeding Research, 50829 Cologne, Germany b Sainsbury Laboratory, John Innes Centre, Norwich NR4 7UH, United Kingdom |
| AuthorAffiliation_xml | – name: b Sainsbury Laboratory, John Innes Centre, Norwich NR4 7UH, United Kingdom – name: a Plant Chemetics Lab, Max Planck Institute for Plant Breeding Research, 50829 Cologne, Germany |
| Author_xml | – sequence: 1 fullname: van der Hoorn, Renier A.L – sequence: 2 fullname: Kamoun, Sophien |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/18723576$$D View this record in MEDLINE/PubMed |
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| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 www.plantcell.org/cgi/doi/10.1105/tpc.108.060194 Address correspondence to hoorn@mpiz-koeln.mpg.de. |
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| PublicationTitle | The Plant cell |
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| Snippet | The Guard Model for disease resistance postulates that plant resistance proteins act by monitoring (guarding) the target of their corresponding pathogen... |
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| SubjectTerms | Arabidopsis Proteins Arabidopsis Proteins - genetics Arabidopsis Proteins - metabolism Arabidopsis Proteins - physiology Carrier Proteins Carrier Proteins - genetics Carrier Proteins - metabolism Carrier Proteins - physiology Cladosporium Cladosporium - physiology disease models Disease resistance Evolution genes genetics Host-Pathogen Interactions metabolism microbiology Mimicry Models, Biological Pathogens Perception Perspective physiology Plant cells Plant Diseases Plant Diseases - genetics Plant Diseases - microbiology Plant immunity Plant pathogens Plant populations plant proteins Plant Proteins - genetics Plant Proteins - metabolism Plant Proteins - physiology Plant resistance Protein Binding Protein Serine-Threonine Kinases Protein-Serine-Threonine Kinases - genetics Protein-Serine-Threonine Kinases - metabolism Protein-Serine-Threonine Kinases - physiology Pseudomonas syringae Pseudomonas syringae - physiology Receptors Virulence Xanthomonas campestris Xanthomonas campestris - physiology |
| Title | From Guard to Decoy: A New Model for Perception of Plant Pathogen Effectors |
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