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How does an understanding of the guard hypothesis change the way we view host-pathogen dynamics

How does an understanding of the guard hypothesis change the way we view host-pathogen dynamics. Both models likely pertain in different specific interactions. Under direct interaction model the pathogen protein is recognized directly

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How does an understanding of the guard hypothesis change the way we view host-pathogen dynamics

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  1. How does an understanding of the guard hypothesis change the way we view host-pathogen dynamics • Both models likely pertain in different specific interactions. • Under direct interaction model the pathogen protein is recognized directly • Under the guard hypothesis the activity of the pathogen protein is recognized. • R-gene may be able to recognise more than one Avr gene, more than one pathogen (Mi gene in tomato) • It may be more difficult to circumvent recognition in the later case.

  2. So what about evolution? • “Guard” R-proteins tend to be under stabilizing or balancing selection • i.e. these genes show little diversity in populations • Direct interactors tend to be under diversifying selection- this applies to both the R-genes and the Avr genes with which they interact. • We really don’t know enough to say whether this is a hard-and-fast rule.

  3. What happens next? • Signal transduction system has not been worked out largely. • Will be looked at in susequent lectures • A number of genes have been identified that play an important role • For the most part these genes are not polymorphic within the host population. • This means that R-genes are effectively responsible for recognitional specificity • But see case of Prf/Pto/AvrPto.

  4. Most plants are resistant to most pathogens • Non-host resistance • Pathogens are specifically adapted to their hosts

  5. Non-Host Resistance is likely based on a number of mechanisms • Some of it may be structural

  6. The plant basal defence system • A relatively recent concept • Plants can recognize certain broadly-conserved molecules associated with pathogens- PAMPs (pathogen-associated molecular patterns) • Also known as MAMPs (microbe-associated…) • Examples include flagellin and elongation factor-Tu

  7. MAMPS are recognized by receptors at the cell surface • Case of Flagellin • Found in many bacteria • Plants have a sensitive perception system for the most conserved domain of bacterial flagellin • Duran et al The Plant J .18(3), 265–276

  8. Abramovitch et al.Nature Reviews Molecular Cell Biology7, 601–611 (August 2006) | doi:10.1038/nrm1984

  9. FLS2, the flagellin receptor was identified in Arabidopsis • FLS2 is a Receptor-like Kinase with a LRR. Identical in overall structure (not sequence) to Xa21 a class 5 R-gene. • Ef-tu (another MAMP) receptor has a similar structure • Fls2 and a subunit of flagellin interact in vitro • Suggests a direct interaction in vitro • Why do you think the guard model might not make sense in this case?

  10. Knockout of the FLS2 receptor increases bacterial susceptibility • To an already virulent pathogen • No increased resistance observed when bacteria injected into leaves • Implication is that FLS2 is part of an ‘early-warning’ system • FLS2 (and other PAMP receptors?) appear to act through similar pathways to R-genes

  11. So what’s the difference between MAMPs and AVR/Effector genes and between MAMP receptors and R-genes?

  12. MAMPs are molecules that are highly conserved and found in a wide range of microbes, pathogens and non-pathogens alike. They do not necssarily play a direct role in pathogenesis • Avr/Effector genes are generally specific to a few species of plant pathogens and play a role in pathogenesis.

  13. Avr/Effector genes often supress MAMP-induced defences (alternatively they may supress other types of defence response.) • There are likely multiple MAMPs recognised by multiple MAMP-receptors at any one time. • MAMP-receptors recognise MAMPs, often (always?) by direct interaction. They are (usually) conserved within a species. • R-genes mediate effector/Avr gene product recognition, often, but not always , through indirect mechanisms. They are usually highly polymorphic within a species

  14. From Brent and Mackey , Ann Rev Phtyopath, 2007 45:399-436

  15. RIN4 again • Conforms to this model

  16. AvrRpm1 and AvrRpt2 inhibit MAMP-induced responses. • Induced by pure flg22 • Allow greater growth of already-virulent bacteria. • Both these proteins target RIN4. • Overexpression of RIN4 inhibits MAMP-induced defense signalling and vice-versa.

  17. Non-host resistance • Not entirely understood • Never will be? • To some extent at least, it may be due to the specific MAMP-receptors each plant species has and the ability of the pathogen to avoid detection by them or to suppress or nullify the associated immune response. • Why don’t pathogens just load up on effectors to get a wider host range? • More Avr targets • Costs of resistance?

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