1 / 19

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

jui
Télécharger la présentation

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

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

  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?

More Related