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Previous lecture. General intro General definitions Qualitative vs Quantitative resistance What distinguishes these?. Gene-for-gene interaction Typical for qualitative resistance Not all qualitative resistance is of the gene-for-gene type Introduced the Cladosporium fulvum/tomato system

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  1. Previous lecture • General intro • General definitions • Qualitative vs Quantitative resistance • What distinguishes these? P. Balint-Kurti Lecture 2

  2. Balint-Kurti lecture 1

  3. Balint-Kurti lecture 1

  4. Balint-Kurti lecture 1

  5. Balint-Kurti lecture 1

  6. Gene-for-gene interaction • Typical for qualitative resistance • Not all qualitative resistance is of the gene-for-gene type • Introduced the Cladosporium fulvum/tomato system • Discovery of specific elicitors P. Balint-Kurti Lecture 2

  7. Reading • Required • Hogenhout et al 2009 MPMI22:115-1122- please read this paper • Recommended • Wroblewski et al Plant Phys 2009 150:1733-1749 • Hass et al 2009 Nature 461:393-398 P. Balint-Kurti Lecture 2

  8. 3 studies- continued P. Balint-Kurti Lecture 2

  9. 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

  10. “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

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

  12. Generation of the Rp1-D21 recombinant 7 8 9 X 7 1 2 3 4 6 9 5 8 Rp1-D21 2/9 1 A dominant lesion mimic mutant

  13. 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

  14. Cell Autonomous Nature of R-genes Balint-Kurti lecture 1 BENNETZEN, J. L., W. E. BLEVINS and A. H. ELLINGBOE, 1988 Cell-Autonomous Recognition of the Rust Pathogen Determines Rp1-Specified Resistance in Maize. Science 241: 208-210.

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

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

  17. Molecular Biology of Gene-for-Gene Interaction • Many R and AVR genes have been cloned P. Balint-Kurti Lecture 2

  18. Cloning of First Avr Genes • 25 years ago • See special anniversary issue of Molecular Plant Pathology 2009, 10:6 P. Balint-Kurti Lecture 2

  19. P. Balint-Kurti Lecture 2

  20. P. syringae race 5 P. syringae race 5 P. syringae race 5 P. syringae race 5 P. syringae race 5 P. syringae race 5 P. syringae race 5 P. syringae race 5 P. syringae race 5 P. syringae race 5 P. syringae race 5 P. syringae race 5 P. syringae race 5 P. syringae race 5 P. syringae race 5 P. syringae race 5 P. syringae race 5 P. syringae race 5 P. syringae race 5 P. syringae race 5 P. syringae race 5 P. syringae race 6 Infect Harosay Soybean and look for HR Genomic Library P. syringae race 5 Avr Avr P. Balint-Kurti Lecture 2

  21. Cloned AvrA No known function (I think) P. Balint-Kurti Lecture 2

  22. Cf-9/Avr9 system Avr9 was cloned by purifying and sequencing the protein and using this info to get to the gene. P. Balint-Kurti Lecture 2

  23. What happens if you express Avr9 transgenically in a Cf9 plant? P. Balint-Kurti Lecture 2

  24. Used transposon tagging to mutate the Cf9 R-gene • Ac is a DNA transposon- “Jumping gene” • Encodes an enzyme that: • Recognizes the borders of Ac • Cuts it out and moves it elsewhere in the genome (usually to linked sites) • Can separate ability to encode enzyme and ability to be moved: • Ds- can be moved by Ac transposase but can’t encode transposase • sAc-can encode transposase but can’t be moved P. Balint-Kurti Lecture 2

  25. Cloning an R-gene P. Balint-Kurti Lecture 2

  26. P. Balint-Kurti Lecture 2

  27. Aside: R-genes are powerful things It’s disastrous to let them fall into the “wrong hands” P. Balint-Kurti Lecture 2

  28. What are AVR genes? • And why does the pathogen have them?? • No common sequence features • -in contrast to R-genes Caveat- they often share export signals: RLXR in Oomycetes- see later • Also in bacteria: Guttmanet al. Science295 “A Functional Screen for the Type III (Hrp) Secretome of the Plant Pathogen Pseudomonas syringae,” P. Balint-Kurti Lecture 2

  29. First clue; HRP genes in plant pathogenic bacteria Hypersenesitive reaction and pathogenicity. Deletion of Hrp genes leads to abolition of both functions. P. Balint-Kurti Lecture 2

  30. What’s going on? Any thoughts? Existence of Hrp genes implies that in bacteria the same processes that control avirulence also condition pathogenicity P. Balint-Kurti Lecture 2

  31. Hrp genes are clustered in the bacterial genome. Many are components of the bacterial Type III secretion system, which can inject proteins into host cells. P. Balint-Kurti Lecture 2 http://www.southalabama.edu/clb/archives/july2006.htm

  32. Many secreted proteins share some sequence features that allow their recognition by the TIIISS. • See review Alfano and Colmer. Ann. Rev. Phytopathol. 2004 42:385-414 P. Balint-Kurti Lecture 2

  33. What are AVR genes? P. Balint-Kurti Lecture 2 • Often act as virulence or effector proteinsin the absence of corresponding R-gene • This explains why pathogens have them in the first place • Avr genes are now more commonly known as effectors.

  34. Effectors • Can be defined a number of ways; • “all pathogen proteins and small molecules that alter host cell structure and function” • Hogenhout et al 2009 MPMI22:115-1122- please read this paper • In fact the term is often used to mean all proteins exported by the pathogen in the host • A function in “altering host cells” is assumed P. Balint-Kurti Lecture 2

  35. Effectors • All (?) Avr genes are effectors • But all effectors are not Avr Genes • Although they are potential Avr genes (see Wroblewski, T., et al. Plant Physiol. 2009;150:1733-1749) P. Balint-Kurti Lecture 2

  36. What kinds of things are these effector proteins doing? We now know that microbial pathogens export a whole arsenal of effector molecules into their host to alter their environment for their purposes. Some effectors are injected into host cells Others go to the apoplast P. Balint-Kurti Lecture 2

  37. What kinds of things are these effector proteins doing? P. Balint-Kurti Lecture 2 • Hogenhout et al MPMI 2009 22:115-122 list the following functions: • Alter plant behavior/development • Suppress plant immunity • Suppress HR • Suppress signalling • Suppress recognition of other AVR genes (see rin4 system) • Protect fungus from host degradative enzymes • E.g. Avr4 is a chitinase inhibitor. • Some cause cell death (CRN effector of oomycetes)

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