The Guard Hypothesis: R proteins function as sensors to “guard” the targets of pathogen effector molecules.
The Guard Hypothesis: R proteins function as sensors to “guard” the targets of pathogen effector molecules.
Another example- Rin 4
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So Rin4 is guarded by at least two R-genes in Arabidopsis; RPM1(mediates AvrB recognition) and RPS2 (mediated AvrRpt2 recognition)
Maybe
Another Example:Pto/AvrPto
Why in this case is Pto rather than Prf identified as the resistance gene?
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Aside:Hybrid Necrosis
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Bomblies et al (2007) Plos Biology 5:e236
Why might Hybrid Necrosis Occur?
How does an understanding of the guard hypothesis change the way we view host-pathogen dynamics
So what about evolution?
A further elaboration
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This is an unstable situation
Evidence
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BS3
What happens next?
Most plants are resistant to most pathogens
Non-Host Resistance is likely based on a number of mechanisms
The plant basal defence system
MAMPS are recognized by receptors at the cell surface