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  • Sliding window analysis of silent (synonymous and noncoding) sites in RPS5 flanking regions. Window size is 250 silent sites with a 25-site increment. Abscissa is base position relative to DJ in aligned sequences. (A) Observed nucleotide diversity between RPS5+ and RPS5− alleles and average divergence between A. thaliana and A. lyrata sequences, with Jukes-Cantor correction (39). (B) Results of a coalescent model with selection and recombination (3, 10). For each sliding window, plotted is the ratio of average pairwise difference between allelic classes (observed or predicted under balancing selection) to average pairwise difference expected under the standard neutral model (see Materials and Methods for details). Results for two scaled recombination rates are shown for balancing selection (BS) predictions: ρ = 6 × 10−4, our best estimate of this parameter, and ρ = 6 × 10−5, a 10-fold lower rate. Both expected curves assume an equilibrium frequency of the two allelic classes, P = 0.5; The scaled mutation rate (β) between RPS5+ and RPS5− is fitted for each curve to bring the predictions close to data at the site under selection (assumed to be the DJ).
  • 2-1-10.ppt - PowerPoint Presentation

    1. 1. Couple of quick things: • Linkage drag
    2. 2. • Needs to be minimized in the introgression of QTL, especially from exotic species • How do we do this?
    3. 3. Tolerance • The ability to maintain yield in the face of high disease/ symptoms – Not necessarily the same as apparent resistance • In the end that’s what we need! • More difficult to score for than resistance
    4. 4. Costs of Resistance
    5. 5. • Why is defence inducible? – Why not induce basal defences constitutively?
    6. 6. Induced resistance can be costly • costly to over do it – Analogous to autoimmune disease • Costly not to do anything though
    7. 7. Fitness Costs of Mutations Affecting the Systemic Acquired Resistance Pathway in Arabidopsis thaliana Heidel et al 2004 Genetics 168, 2197-2206
    8. 8. Field Greenhouse High nutrient low nutrient Constitutive defense gene expression Low defence gene induction
    9. 9. How about R-genes? • Why are R-genes polymorphic within a species anyway? • Avr genes are polymorphic • But why doesn’t each plant keep a full complement of R-genes? – Presumed advantage in the presence of the corresponding Avr gene – How about in its absence?
    10. 10. Maintaining R-genes may be costly • In the absence of the corresponding pathogen • Tian, D., Traw, M.B., Chen, J.Q., Kreitman, M., and Bergelson, J. (2003). Fitness costs of R-gene-mediated resistance in Arabidopsis thaliana. Nature 423, 74-77.
    11. 11. How to compare plants with/without a resistance gene • Need isogenic lines • Could create NILs by conventional back- crossing – But the plants would differ for a large locus containing many genes – Difficult to attribute change in phenotype to any single gene
    12. 12. How to compare plants with/without a resistance gene • Can transform a susceptible line. – But the insertion of a transgene may itself have an effect
    13. 13. Used a Cre/lox system http://www.i-med.ac.at/phd/neuroscience/lectors/christoph_schwarzer.html Rpm1 gene Able to create two completely isogenic lines differing for just Rpm1
    14. 14. Looked at presence/absence of RPM1
    15. 15. • A 9% fitness cost • Is this a common occurrence? • Rps5 has a similar cost (J.Bergelson pers. com.)
    16. 16. Rpw8 has a cost in absence of pathogen • Undral et al 2007 Intraspecific Genetic Variations, Fitness Cost and Benefit of RPW8, A Disease Resistance Locus in Arabidopsis thalianaGenetics176, 2317-2333 • In this paper they just compared transgenic and non-transgenic lines
    17. 17. WildType TransgenicexpressinRpw8 Disease pressure No Disease
    18. 18. Some of the transformants looked like this
    19. 19. Why might this occur • Metabolic costs of expressing another gene – Unlikely – ~30,000 genes in Arabidopsis • Inappropriate activation of R-genes – Possible – See hybrid necrosis and evidence from Rpw8
    20. 20. R-protiens require other host factors for proper folding SangsterandQueitsch2005TheHSP90chaperone complex,anemergingforceinplantdevelopmentand phenotypicplasticityCurrentOpinioninPlantBiology 8;86-92
    21. 21. • In hybrid necrosis it appears that the introduction of functional R-genes into a novel genetic background may lead to mis-regulation of their activity. • Maybe this type of thing occurs often with the R genes in their natural background but at much lower levels.
    22. 22. Other evidence for this phenomenon • There are two reasons we might see polymorphism in a natural population – One allele might be rising in a pop and the other falling and we have caught the population “in transition” – Or it’s a stable situation-balancing selection
    23. 23. Time FrequnecyFrequnecy Directional selection (selective sweep) Balancing selection Timeofsampling
    24. 24. • Balancing selection implies different alleles are beneficial in different situations • Can identify “signatures” of balancing selection – If the two alleles are recently diverged there should be few polymorphisms in the regions surrounding them – If the two alleles have been maintained separately for a long time there should be lots of polymorphism in the region surrounding them
    25. 25. Sliding window analysis of silent (synonymous and noncoding) sites in RPS5 flanking regions Tian D et al. PNAS 2002;99:11525-11530 ©2002 by National Academy of Sciences Do not ask me about this graph! Similar study showed similar results for Rpm1: Stahl et al 1999 Nature 400:667-671
    26. 26. • Surely these must be exceptions • >100 RGAs in Arabidopsis, they can’t all have a yield penalty! – Rps5, Rpw8 and Rpm1 seem to have significant costs, – but other studies on RPS2 and RPP5 do not give similar results. No fitness cost of the R- genes in absence of disease • Korves and Bergelson2004 A Novel Cost of R Gene Resistance in the Presence of Disease Am Nat 163: 489–504 • Caveat , it’s a little more complicated than this!
    27. 27. Bergelson pers. com. • “the key here is that the costs are required for long-lived polymorphisms. Rpm1, for example, looks to be an ancient balanced polymorphism and therefore we expect costs.” • “There are lots of R genes that are not balanced polymorphisms, but instead have relatively young alleles. You can see a range of evolutionary trees by looking at our Plant Cell paper” – Bakkera et al 2006 A Genome-Wide Survey of R Gene Polymorphisms in Arabidopsis[The Plant Cell 18:1803-1818 (2006)
    28. 28. Are all R-genes polymorphic anyway? • If there is no fitness cost they would likely go to fixation in the population • If they are fixed, how would we detect them? • Possibly many (most?) RGAs are like this, I don’t think it’s really been investigated. • Would need the genomic sequence of multiple genomes of different lines. • Difficult to investigate as it’s tricky to tell what is functionally important polymorphism and what isn’t
    29. 29. Costs of Quantitative Risistance • Genetics of Brassica rapa. 3. Costs of Disease Resistance to Three Fungal Pathogens Mitchell-Olds and Bradley 1996 Evolution, 50, 1859-1865 • Recurrently selected for quantitative levels of disease Recurrently selected for quantitative levels of disease resistance
    30. 30. • Again, there are several other studies that do not show this effect.
    31. 31. • This is an area requiring further work • When you select for higher yield might you be creating lines with lower resistance? • When you select for increased resistance might you be creating lines with lower yield?