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Qualitative Disease Resistance

Qualitative Disease Resistance. aka: Vertical; Qualitative; Inoculum-reducing; Major-effect; Hypersensitive; Monogenic; ‘R’ gene.Complete Race-specific Single gene “Vertical” Gene-for-gene . 100% severity. Amount of disease. 0% severity. Race 1. Race 2. Race 3. Race 4.

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Qualitative Disease Resistance

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  1. Qualitative Disease Resistance aka: Vertical; Qualitative; Inoculum-reducing; Major-effect; Hypersensitive; Monogenic; ‘R’ gene.Complete Race-specific Single gene “Vertical” Gene-for-gene 100% severity Amount of disease 0% severity Race 1 Race 2 Race 3 Race 4 Balint-Kurti lecture 1

  2. Balint-Kurti lecture 1

  3. Quantitative Disease Resistance aka: Horizontal; Rate-reducing; Minor-effect; General; Polygenic; Additive; Incomplete, Partial Race-nonspecific Multi-genic Balint-Kurti lecture 1

  4. Balint-Kurti lecture 1

  5. Balint-Kurti lecture 1

  6. Balint-Kurti lecture 1

  7. Biotrophic pathogens • Derive nutrition from living host cells, Usually establish a long-term interaction with the plant. • Necrotrophic pathogens • Kill host cells. Derive nutrition from dead cells Balint-Kurti lecture 1

  8. The Molecular Basis of Qualitative/Major gene resistancea chronological summary Balint-Kurti lecture 1

  9. 1940’s H. H. Flor Balint-Kurti lecture 1 MOLECULAR PLANT PATHOLOGY 8 349–364

  10. Pathogen Host Balint-Kurti lecture 1

  11. Pathogen AVR1AVR2 AVR1avr2 avr1AVR2 avr1avr2 R1-R2- Incompatible (Resistant) Incompatible (Resistant) Incompatible (Resistant) Compatible (Susceptible)  R1-r2r2  Incompatible (Resistant) Incompatible (Resistant) Compatible (Susceptible)  Compatible (Susceptible) Host r1r1R2-  Incompatible (Resistant) Compatible (Susceptible)  Incompatible (Resistant) Compatible (Susceptible) r1r1r2r2 Compatible (Susceptible) Compatible (Susceptible) Compatible (Susceptible) Compatible (Susceptible) Balint-Kurti lecture 1

  12. What does this mean? • Implies, interaction (direct of otherwise) of dominant Resistance and Avirulence gene products leads to resistance. • The loss of an AVR gene in the pathogen can render the corresponding R gene essentially useless. • It doesn’t matter how many interactions there are leading to compatibility. A single R/Avr match will lead to resistance. Balint-Kurti lecture 1

  13. What did classical genetics tell us? • Gene-for-gene interactions were identified in many different interactions with many different types of pathogens • R-genes were often clustered in “complex loci.” • Avr genes were not clustered • What does this suggest to you? Balint-Kurti lecture 1

  14. Predictions • Pathogen is ‘trying to lose’ Avr genes. • Why does a pathogen have AVR genes in the first place? • Host is ‘trying to develop’ new types of R genes Balint-Kurti lecture 1

  15. What was known about R-genes? • Often associated with hypersensitive response (HR) • In some cases, usually where complex loci are involved, they were quite unstable. Balint-Kurti lecture 1

  16. Three elegant studies • Confirms our understanding of Gene-for-Gene • Helps us understand R-gene structure and variability • Helps us understand R-gene function Balint-Kurti lecture 1

  17. Elicitors from the Cladosporium fulvum/ tomato system • Pierre de Wit • Several Avr/R gene interactions were characterized • Avr2/Cf2 • Avr4/Cf4 • Avr5/Cf5 • Avr9/Cf9 http://www.php.wur.nl/UK/Research/Cladosporium/?wbc_purpose=Basic&WBCMODE=PresentationUnpublished/#avr Balint-Kurti lecture 1

  18. Fungus grows strictly in the apoplastic space- doesn’t invade host cells • Can you isolate Avr elicitors from apoplastic fluid Balint-Kurti lecture 1

  19. Cf2 Cf4 Isolate intercellular fluid and inject into Cf2, Cf4, Cf5 Cf9 leaves Cf5 Cf9 http://www.php.wur.nl/UK/Research/Cladosporium/ Balint-Kurti lecture 1

  20. Balint-Kurti lecture 1

  21. Conclusions • Identified specific elicitors associated with R-gene-mediated defense response. • Specific peptide elicitors were identified from intercellular fluid • Don’t necessarily need pathogen itself to be present to invoke R-gene mediated resistance Balint-Kurti lecture 1

  22. Unstable nature of R-genes • Seems to be associated with meiosis • R-genes don’t spontaneously cease functioning in an existing plant. Balint-Kurti lecture 1

  23. “tester” - no R gene Homozygous for R gene, heterzygous for flanking markers a A a A Select susceptible progeny r X r OR R R 25/15,646 b b B B 24/25 show non-parental combinations Sudapak et al, 1993 Genetics, Vol 133, 119-125 Balint-Kurti lecture 1

  24. Sudapak et al, 1993 Genetics, Vol 133, 119-125 Balint-Kurti lecture 1

  25. Conclusion • Complex nature of R-gene loci leads to their unstable nature. • NB many , but not all, R-genes occur in complex loci. Balint-Kurti lecture 1

  26. Cell Autonomous Nature of R-genes Balint-Kurti lecture 1

  27. Developing maize embryo’s were exposed to X-rays rp1 Rp1 rp1 oy Oy oy Balint-Kurti lecture 1

  28. HR in green sectors • Pustules in yellow sectors • HR doesn’t cross into yellow sectors (much-1F). • Rp1 is not diffusible Balint-Kurti lecture 1

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