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Race Specificity of disease resistance QTL

Race Specificity of disease resistance QTL. Genetic selection and adaptation of Cochliobolus heterostrophus to corn hosts with partial resistance. Kolmer and Leonard Phytopathology. 76:774-777. 1986. Recurrently selected for virulence of C. heterostrophus on one line- 316.

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Race Specificity of disease resistance QTL

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  1. Race Specificity of disease resistance QTL • Genetic selection and adaptation of Cochliobolus heterostrophus to corn hosts with partial resistance. Kolmer and Leonard Phytopathology. 76:774-777. 1986. • Recurrently selected for virulence of C. heterostrophus on one line- 316. P Balint-Kurti QDR lecture

  2. Saw line-specific as well as line-non-specific response. • What does this mean? • Probably there is isolate-specific as well as general resistance at play here P Balint-Kurti QDR lecture

  3. Do these dichotomies really exist? P Balint-Kurti QDR lecture

  4. Is quantitative resistance really durable? • This is certainly the received wisdom though few formal studies have been done (?) • Likely to be true • But some major genes Lr34 and Sr2 for instance are durable too. P Balint-Kurti QDR lecture

  5. Do these dichotomies really exist? P Balint-Kurti QDR lecture

  6. True, but major genes might also be developmentally and environmentally influenced. • At temperatures above 28°C, the HR and the restriction response associated with the tobacco N gene become inactive. P Balint-Kurti QDR lecture

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  8. Do these dichotomies really exist? P Balint-Kurti QDR lecture

  9. (almost) all available necrotrophic resistance is quantitative P Balint-Kurti QDR lecture

  10. Do these dichotomies really exist? P Balint-Kurti QDR lecture

  11. Quantitative resistance is, by definition, partial • But some (most?) R-genes do not confer complete resistance either. P Balint-Kurti QDR lecture

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  13. Lots of examples of this type of thing Randy Wisser P Balint-Kurti QDR lecture

  14. “Ghost” effects • Defeated R-genes still seem to be doing something! P Balint-Kurti QDR lecture

  15. So are Quantitative resistance genes similar to major R-genes? • Maybe… • Most of the perceived differences are matters of degree • Rcg1, a quantitative gene for anthracnose stalk rot resistance was cloned and found to encode an NBS-LRR gene. • But Rcg1 has an extremely significant effect • What is the difference between a “major” gene and a strong QTL? P Balint-Kurti QDR lecture

  16. Perhaps R-genes products that interact weakly with their corresponding Avr genes products/ guardee proteins cause partial resistance? • There is some evidence for this. E.g. weak interactions between L gene products in flax and corresponding Avr gene products is associated with weaker HR response • Presumably this happens often during evolution P Balint-Kurti QDR lecture

  17. QTL disproportionately colocalize with RGA in rice P Balint-Kurti QDR lecture

  18. Integrated disease-QTL map of rice • disease QTL • R-genes • RGAs (NBS-LRR) • Lesion mimic genes Randy Wisser Wisser et al., 2005 Genetics Wisser et al. 2005 Genetics 169: 2277 P Balint-Kurti QDR lecture

  19. R-genes can’t be the whole story surely! • What other types of things might cause variations in quantitative resistance? • Structural features • Cell wall • Stomatal density, openness • Preformed defenses • Phytoalexins etc. • Components of the basal defence system? • PAMP receptors? • Effector targets? P Balint-Kurti QDR lecture

  20. Traits affecting leaf wetness may play a role • In fact there are likely lots of factors that will alter the extent to which a susceptible plant is infected and the level of symptoms displayed. P Balint-Kurti QDR lecture

  21. Cloned Quantitative Disease Resistance Genes • Recently four publications have reported the cloning of quantitative resistance genes P Balint-Kurti QDR lecture

  22. Fu et al. 2009. A Kinase-START Gene Confers Temperature-Dependent Resistance to Wheat Stripe Rust. Science 323:1357-1360. • Yr36 (WKS1), which confers resistance toa broad spectrum of stripe rust races at relatively high temperatures(25° to 35°C) • Associated with durable resistance P Balint-Kurti QDR lecture

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  24. “The WKS1 protein contains a steroidogenic acute regulatory protein-related lipid transfer domain (START) and a functional enzymatic (kinase) domain, suggesting a role for plant lipids in cell signaling” Kliebenstein and Rowe 2009 Science 323:1301-2 required reading P Balint-Kurti QDR lecture

  25. Krattinger et al. 2009. A Putative ABC Transporter Confers Durable Resistance to Multiple Fungal Pathogens in Wheat. Science 323:1360-1363. • Confers resistance to multiple rusts and a mildew • Partially dominant • Lr34 has supported resistance to these pathogensfor more than 50 years. • Durable, multiple disease resistance • Flag leaves of many wheatcultivars containing Lr34 develop a necrotic leaf tip, a morphologicalmarker described as leaf tip necrosis P Balint-Kurti QDR lecture

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  28. Encodes an ABC transporter. • This class of genes move diverse products across plant membranes • “it is possible that Lr34 resistance is the result of senescence-likeprocesses. Alternatively, LR34 may play a more direct role inresistance by exporting metabolites that affect fungal growth” P Balint-Kurti QDR lecture

  29. Manosalva, et al. 2009. A Germin-Like Protein Gene Family Functions as a Complex Quantitative Trait Locus Conferring Broad-Spectrum Disease Resistance in Rice. Plant Physiol. 149:286-296. • Confers resistance to rice blast and sheath blight • Actualy resistance hasn’t been associated with a single gene, but with a set of 8 related genes • “The mechanism by which GLPs influence plant defense is likelyrelated to their generation of active oxygen species.” P Balint-Kurti QDR lecture

  30. Fukuoka et. Al 2009 Loss of Function of a Proline-Containing Protein Confers Durable Disease Resistance in Rice Science 325: 998 - 1001 • Confers resistance to rice blast • “Pi21 has maintainedresistance throughout a century of cultivation” • “Wild-type Pi21 appears to slow the plant’sdefense responses, which may support optimization of defensemechanisms. “ • PI21 is a dominant susceptibility allele conferring partial susceptibility.. A proline-rich gene of previously unknown type • “The rate of penetration of hyphaeinto host cells in AA-pi21 did not differ from that in AA but the rate of invasion of hyphae from penetrated cells intoadjacent cells, as an indicator of hyphal growth, was significantlylower in AA-pi21 “ • In pi21 plants a slow cell death appears to be triggered on infection- slower than HR P Balint-Kurti QDR lecture

  31. pi21 PI21 P Balint-Kurti QDR lecture

  32. What does this tell us? • Supports the idea that QDR may be conferred by lots of different types of genes • Not just RGAs • In these cases resistance was to biotrphic or hemi-biotrophic pathogens • In 3 of the 4 examples, control of programmed cell death/ senescence may be the key characteristic P Balint-Kurti QDR lecture

  33. Is quantitative resistance effective against multiple diseases • This area has not been looked at much. • If the resistance mechanism is somewhat general then you might expect it to be effective against a set of similar pathogens. • Mitchell-Olds, T., R. V. James, M. V. Palmer, and P. H. Williams, Genetics of Brassica rapa (syn. campestris). 2. Selection for multiple disease resistance to three fungal pathogens: Peronospora parasitica, Albugo candida, and Leptosphaeria maculans,Heredity, vol. 75 (1995), pp. 362-369 . P Balint-Kurti QDR lecture

  34. Positive correlations among multiple diseases Southern leaf blight Northern leaf blight Gray leaf spot R. J. Wisser P Balint-Kurti QDR lecture

  35. So what use are dQTL? • Knowledge of the location of disease resistance QTL can be used in “Marker Assisted Breeding” (MAS). • MAS uses markers to follow and incorporate into germplasm previously mapped genes for a beneficial phenotype • But… • Quantitative resistance can be incorporated by simple selection without knowledge of QTL positions P Balint-Kurti QDR lecture

  36. Jim Holland Catch-22 of MAS If phenotypic data are poor indicators of genotypes, you cannot adequately map QTLs to implement MAS. If phenotypic data are good, you do not need MAS. P Balint-Kurti QDR lecture

  37. Jim Holland The Catch-22 can be avoided if: • A small number of QTLs explain most of the genetic variation, in which case: • High heritability in the QTL mapping phase is optimal to identify QTL markers, then: • Markers can be implemented more easily/cheaply than phenotyping in future selection cycles. P Balint-Kurti QDR lecture

  38. In other words… • MAS makes sense: • If QTL mapping is accurate. • And the QTL being selected for have reasonably large effects • And if it is difficult/costly to select directly for resistance • Under what circumstances would this happen? P Balint-Kurti QDR lecture

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