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Most plants are resistant to most pathogens

Most plants are resistant to most pathogens. Non-host resistance Pathogens are specifically adapted to their hosts. Non-Host Resistance is likely based on a number of mechanisms. Some of it may be structural. The plant basal defence system. A relatively recent concept

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Most plants are resistant to most pathogens

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

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

  3. 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

  4. 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

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

  6. FLS2, the flagellin receptor was identified in Arabidopsis (Mol. Cell 5:1003-1011) • 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? (for the host that is)

  7. Knockout of the FLS2 receptor increases bacterial susceptibility (Zipfel et al.(2004). Bacterial disease resistance through flagellin perception in Arabidopsis. Nature, 428: 764-767) • 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 activate similar responses to R-genes • But at a lower level

  8. Class 4 Class 2 Class 3 Prf Class 5 Class 1 Plant pathogens and integrated defence responses to infection Jeffery L. Dangl and Jonathan D. G. Jones Nature 411, 826-833(14 June 2001) P. Balint-Kurti Lecture 4

  9. AvrPto inhibits FLS2 action • Xiang et al 2008 Curr Biol.18:74-80. Pseudomonas syringae effector AvrPto blocks innate immunity by targeting receptor kinases. • Inhibits the kinase of FLS2 in a similar way to its interaction with Pto P Balint-Kurti QDR lecture

  10. Class 4 Class 2 Class 3 Prf Class 5 Class 1 Plant pathogens and integrated defence responses to infection Jeffery L. Dangl and Jonathan D. G. Jones Nature 411, 826-833(14 June 2001) P. Balint-Kurti Lecture 4

  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 necessarily 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. Often are exported into host cells or into the apoplast

  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 • May conform to this model • Cell 2005 121:749-759

  16. AvrRpm1 and AvrRpt2, which both target RIN4, inhibit MAMP-induced responses Induced by pure flg22 • Allow greater growth of already-virulent bacteria. • Overexpression of RIN4 inhibits MAMP-induced defense signalling and vice-versa. • Is RIN4 an inhibitor of MAMP-induced signalling?

  17. Non-host resistance • Not entirely understood • There are likely myriad causes • 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 • Metabolic costs • It appears that P. infestans might be doing this- it’s a formidable pathogen

  18. Quantitative Disease Resistance • It is probable that most disease resistance used in cultivated crops is quantitative rather than qualitative • Arguably , this applies generally, or it will in the future. • Very little is known about physiological or molecular genetic basis of quantitaive disase resistance P Balint-Kurti QDR lecture

  19. P Balint-Kurti QDR lecture

  20. Host-pathogen interactions: individual-level SUSCEPTIBLE RESISTANT SUSCEPTIBLE RESISTANT SUSCEPTIBLE RESISTANT SUSCEPTIBLE RESISTANT Host-pathogen interactions: population-level Host genotype Pathogen genotype Randy Wisser P Balint-Kurti QDR lecture

  21. Quantitative trait loci (QTL) control quantitative traits P Balint-Kurti QDR lecture

  22. Quantitative trait loci are genetic loci which are associated with a change in the trait under investigation. • One or more linked genes may underlie a QTL P Balint-Kurti QDR lecture

  23. Finding dQTL P Balint-Kurti QDR lecture

  24. Why are we interested in Quantitative Resistance? • After all, major-gene resistance gives higher resistance and is easier to manipulate. • Durability • Resistance to necrotrophic pathogens • Quantitative disease resistance to biotrophic pathogens exists also • But there is no (very little?) major-gene resistance to most necrotrophs. P Balint-Kurti QDR lecture

  25. What do we know about Quantitative Resistance? • We have mapped a lot of QTL • A few genes have now been cloned • More on this later • Not much else • Yet it is arguably the most important form of resistance used in breeding • Why is there this lack of knowledge? P Balint-Kurti QDR lecture

  26. Disease Resistance QTL are everywhere! • >89% of maize genome covered P Balint-Kurti QDR lecture

  27. Why? • Lots of Diseases • Lots of Genes • Lots of imprecision • Some genes are mapped inaccurately • Most genes are mapped imprecisely P Balint-Kurti QDR lecture

  28. Is the dogma true- do these dichotomies really exist? P Balint-Kurti QDR lecture

  29. Is this dogma true- do these dichotomies really exist? P Balint-Kurti QDR lecture

  30. Is quantitative resistance really non-race –specific? • Several publications suggest that some QTL are race specific • Marcel et al looked at Barley leaf rust system. • Suggested that some of the smaller effect QTL are race-specific • Suggested the existence of a minor gene –for-minor gene interaction P Balint-Kurti QDR lecture

  31. In this case detection of race-specific QTL depended on how the analysis was done P Balint-Kurti QDR lecture

  32. P Balint-Kurti QDR lecture

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