Topic 1 how do pathogen pest populations respond to deployment of host resistance
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Topic 1 : How do pathogen/pest populations respond to deployment of host resistance?. Natural vs. human-managed systems Selective effects of qualitative resistance (R genes) How does evolution to virulence affect pathogens – is there a cost to virulence?

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Topic 1 how do pathogen pest populations respond to deployment of host resistance l.jpg
Topic 1: How do pathogen/pest populations respond to deployment of host resistance?

  • Natural vs. human-managed systems

  • Selective effects of qualitative resistance (R genes)

    • How does evolution to virulence affect pathogens – is there a cost to virulence?

    • Can durability of R genes be predicted?

  • Selective effects of quantitative (partial) resistance

  • Evolution of pathogen populations with host-selective toxins (HSTs)

  • What affects evolutionary potential of pathogen populations

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Pathogen populations evolve differently in human-influenced systems

  • R-gene breakdowns in agricultural systems tend to be dramatic and relatively complete

    • In artificial systems, humans constrain host evolution, deploy R genes in vast swaths

    • Pathogens evolve virulence

    • Humans deploy new R genes

    • Etc.

Comomnly deployed wheat powdery mildew pm resistance genes in nc l.jpg
Comomnly deployed wheat powdery mildew ( systemsPm) resistance genes in NC

% isolates virulent

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Less commonly deployed systemsPm genes in NC

% isolates virulent

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How does evolution to virulence affect pathogens? systems

  • Is there a “cost to virulence” – a fitness cost to having a virulence gene?

  • Vanderplank, 1963 & 1968:

    • Releasing a new R gene causes directional selection: virulent pathotypes increase in frequency

    • When R gene is defeated, withdrawing it from production leads to “stabilizing selection”: pathogen races with unnecessary virulence genes are eliminated

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Types of natural selection systems

Step 1

Step 2

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What is pathogen fitness? systems

  • The combined ability of an organism to survive and reproduce

  • Quantifiable

    • Reproductive rate

    • Infection efficiency

    • Aggressiveness (amount of disease caused)

      • Disease severity

      • AUDPC

    • Frequency of a strain relative to other strains can be used as an estimator of fitness

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Estimating fitness systems

Genotype A: 10 lesions/lesion/day

  • Fitness (W) is a relative parameter -- expressed relative to the most fit genotype (with fitness = 1.0)

    • Relative fitness of B = WB: 0.9

Genotype B: 9 lesions/lesion/day

  • Selection coefficients (s) are also compared to estimate changes in fitness of isolates over time; they measure the intensity of natural selection on a genotype

    • Selection coefficient = the proportion by which the fitness of a genotype is less than that of the most fit

    • Selection coefficient (s) of most fit (most frequent strain) is set to 0, so its W = 1. Relative fitness of other isolates is 1 – s.

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For example: systems(Zhan et al, 2002, Local adaptation and effect of host genotype on the rate of pathogen evolution: an experimental test in a plant pathosystem. J. Evol. Biol. 15:637-647)

  • Question: Is reproductive fitness of a fungal isolate correlated with aggressiveness of that isolate?

  • Method: “Mark-release-recapture” -- co-inoculate multiple strains in equal proportions early in season, let them compete throughout season

    • Measure end-of-season frequencies; most fit strain is inferred to be highest-frequency strain

    • Calculate selection coefficient of Gi (the ith genotype):

      si = 1 - pit pj0


  • Where p = frequency, t = time, and 0 = inoculation time

  • 0 ≤ s ≤ 1.

  • Selection coefficient measures the intensity of selection on that genotype (larger s = higher negative selection against that genotype). Fitness = 1 – s.

pjt pi0

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Madsen systems


Fitness measured in field; aggressive-ness measured in greenhouse

Was aggressive-ness correlated with fitness?


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Is there a cost to virulence? systems

  • How dissociate effect of virulence gene from pathogen’s genetic background?

    • Near-isogenic lines (NILs) of pathogen (Leonard, 1977, Phytopathology 67:1273-1279; Klittich & Bronson,1986, Phytopathology 76:1294-1298)

    • Averaging over large isolate collection (Leonard, 1969, Phytopathology 59:1851-1857)

    • Crosses to dissociate virulence alleles from genetic background (Bronson & Ellingboe, 1986, Phytopathology 76:154-158)

    • Mutants (Prakash & Heather, 1986, Phytopathology 76:266-269)

    • Genetic transformation (Keller et al., 1990, Phytopathology 80:1166-1173)

    • Site-directed mutagenesis (Lindemann and Suslow, 1987, Phytopathology 77:882-886)

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Earl systems

Xi et al. , 2003, Mycol. Res. 107:1485-1492

Fig. 1. Frequency of pathotypes E97-2 and H97-2 of Rhynchosporium secalis co-inoculated over 4 cycles on two barley cultivars: (a) ‘Earl,’ susceptible to E97-2, and (b) ‘Harrington,’ susceptible to both.

E97-2 had complex virulence (to Earl, Harrington, and 5 more cvs).

H97-2 had simple virulence (to Harrington and 1 other cv, not Earl).


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  • “E97-2, systemsa pathotype with unnecessary virulence genes against a susceptible cultivar, had greater parasitic fitness compared with H97-2, a pathotype without unnecessary genes for virulence.” (Xi et al)

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Contrary evidence from malaria parasite systems

  • In 1993, Malawi became the first country in Africa to replace chloroquine with the combination of sulfadoxine and pyrimethamine for the treatment of malaria.

  • At that time, the clinical efficacy of chloroquine was less than 50%.

  • Molecular marker for chloroquine-resistant Plasmodium subsequently declined in prevalence and was undetectable by 2001

  • Chloroquine once again effective in Malawi.

  • How did the frequency of the drug-resistant allele change in Plasmodium?

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Different loci impose different fitness costs systems

Bahri et al, 2009. Tracking costs of virulence in natural populations of the wheat pathogen, Puccinia striiformis f. sp. tritici. BMC Evol. Bio. 9:26.

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So: if you remove a defeated R gene from commercial production, will the corresponding virulence in the pathogen population decline in frequency?

  • One would expect this to happen IF virulence carries a fitness penalty

  • It’s assumed by some:

    • E.g.,“Deployment of disease resistance genes by plant transformation – a ‘mix and match’ approach,” Pink and Puddephat, 1999, Trends in Plant Science, 4:71-75

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“A great advantage of the strategy is that production, will the corresponding virulence in the pathogen population decline in frequency?it does not depend upon a supply of new resistance genes….Existing resistance genes can be recycled. For example, if a gene, or gene combination, is withdrawn because the frequency of the matching virulence increases in the pathogen population it can be re-introduced when thefrequency of the matching virulence allele(s) reduces.” (Pink & Puddephat)

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Best guess: production, will the corresponding virulence in the pathogen population decline in frequency?

  • In general, if R gene is removed from use, frequency of virulence may decrease, but will likely remain sufficient to “flare up” again if R gene is redeployed

  • But magnitude of fitness penalty and length of time needed to restore fitness via compensatory mutations probably varies from virulence mutation to virulence mutation

  • So R genes may vary in durability (compared “head to head,” i.e., deployed on equal acreage, etc.)

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Fitness modifiers / compensatory mutations production, will the corresponding virulence in the pathogen population decline in frequency?

  • Restoration of fitness may occur in the virulence gene itself (further mutations)

  • Or may occur indirectly in other genes determining aggressiveness / fitness

    • Insecticide resistance in Australian sheep blowfly (McKenzie and Purvis, 1984, Chromosomal localisation of fitness modifiers of diazinon resistance genotypes of Lucilia Cuprina, Heredity 53:625-634)

    • Streptomycin resistance in E. coli(Morell, 1997. Antibiotic resistance: road of no return. Science 278:575-576)

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Non-obligate pathogens: selection operates on all phases of life cycle

Morris et al, 2009. Expanding the paradigms of plant pathogen life history and evolution of parasitic fitness beyond agricultural boundaries, PLoS Pathogens 5:1,

  • “Dual-use” traits: have dual roles in environmental (e.g., rhizosphere or phyllosphere) and parasitic fitness

    • Toxins and toxin transport systems: e.g., efflux pumps in Botrytis cinerea confer resistance to antimicrobials from soil and plant microflora, and resistance to plant phytoalexin resveratrol

  • “Exaptation”: virulence can arise or shift via cooptation of phenotypes arising from natural selection unrelated to interaction with host plant

    • Environment – biotic and abiotic stresses

      • Streptomyces bacteria live in soil; apparently some have evolved saponinases, which can confer virulence, to counter saponins produced by plant roots

      • Saprophytic phase – e.g., Fusarium mycotoxins’ role against competitors

    • Basic housekeeping genes

      • Kinesins in Ascochyta rabiei, fungal pathogen of chickpea

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Is there some way to predict durability of particular R genes?

  • Leach et al, 2001. Pathogen fitness penalty as a predictor of durability of disease resistance genes, Annu. Rev. Phytopathology 39:187-224.

    • Reviews evidence related to hypothesis that durability of a resistance gene is a function of the amount of fitness penalty imposed on pathogen.

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Differences in durability of single-gene mediated resistance genes?

  • Some single R genes have proven durable –

    • Monogenic resistance to Fusarium oxysporum in crucifers has lasted 90 yrs

    • Lr34 resistance to wheat leaf rust (Puccinia triticina) has lasted over 30 yrs

  • Xa3, Xa4 resistance in rice to Xanthomonas oryzae durable 10-15 yrs before virulence emerged, still has some effect.

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Some avr genes contribute to fitness genes?

  • Bacteria: Some avr genes control both virulence and avirulence (both elicitors of HR and agents of pathogenicity)

    • Xanthomonas spp. (bacterial pathogens of pepper, tomato, citrus, etc.)

      • avrBs2 -> protein that’s secreted into plant cells; avrBs3 family -> ability to multiply intercellularly; lesion length

    • Pseudomonas syringae pv. tomato

      • avrRpt2 -> blocks activation of defense responses

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Fungal genes with dual function in virulence and avirulence - necrotrophs

  • Cladosporium fulvum (tomato pathogen)

    • Elicitors Avr4, Avr9: Avr4 protects pathogen against chitinase (van den Burg et al, 2006, MPMI, 19:1420–1430)

  • Rynchosporium secalis (barley scald)

    • NIP1 = AvrRs1: kills host cells, releases nutrients

  • Magnaporthe grisea (rice blast)

    • AVR-Pita -> protease expressed after pathogen is inside plant; fitness function unclear

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Avr genes and fitness (summary) - necrotrophs

  • Not all avirulence genes make a measurable contribution to fitness

    • Mutations in Xanthomonad genes avrXa10 and avrBs3 did not cause measurable loss in aggressiveness

  • Some do, and relative magnitude of contribution to fitness may vary, even within highly similar gene family

    • avrXa mutants to virulence exhibit different fitnesses (discussed later)

  • Avr genes may contribute to different fitness attributes

    • Intercellular multiplication

    • Exit of intercellular spaces to leaf surface, etc.

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So if avr genes affect fitness differentially, mutations in them should differentially affect fitness, and R genes corresponding to them should be differentially durable.

  • Fitness penalty due to loss of avr function may be compensated by functional redundancy

    • There may be many copies (e.g., PWL genes in M. grisea, or avrBs3 genes in xanthomonads) some functioning as fitness but not recognition factors, or vice versa

  • Some of structural requirements for fitness and avirulence may be different – it may be possible to lose avirulence function without losing virulence function

    • AvrPto single amino-acid mutants lost avr but not vir function

  • In some cases, amount of avirulence protein can be down-regulated to avoid induction while maintaining virulence function

    • Phytophthora parasitica produces v low levels of elicitin

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Can we PREDICT which R genes will be more/less durable? Example #1:

  • Bai et al knocked out individual avr genes in X. oryzae (2000, MPMI 13:1322-1329).

  • Assayed isolates for fitness (also growth on IR24 leaves, not shown)

  • Avr gene with biggest effect on fitness predicted to correspond to R gene with greatest durability: which one? avrXa7

Tested in field with NILs, natural inoculum. Over 3 yrs, durability of Xa7 > Xa10.

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Example #2: Example #1:

  • Laugé et al: screen for elicitors (avr products) that are important virulence factors, then search for resistance (1998, PNAS 95:9014-9018)

    • Knew avr4 and avr9 could be knocked out without detectable fitness penalty (Cladosporium fulvum on tomato)

    • Knew ECP2 was important virulence factor because ECP2 knockouts only weakly pathogenic

    • Identified 21 lines with resistance beyond known R genes, challenged them with ECP2: 4 had HR

    • If virulence and avirulence do not involve separate domains in ECP2, new R gene Cf-ECP2 expected to be durable