evolution of virulence in plant host- pathogen metapopulation · evolution of virulence in plant...

Evolution of Virulence in Plant Host-Pathogen Metapopulation Peter H. Thrall and Jeremy J. Burdon (2003)

Introduction

§  Infectious diseases à major influence on demography of host populations

§  Variation in host resistance important on disease incidence and prevalence.

§  Negative relationship between host diversity and disease incidence

§  Gene for gene paradigm à Host-pathogen coevolution

Lunedì, 16 novembre 15 2 D-USYS/Agrarwissenschaften/ Gioele Fiori, Christjohannes Gilli

Virulence

§  Individum level:

§  Ability of a pathogen to overcome a given host restance gene.

§  Population level:

§  Average ability of pathogen population to overcome the diversity of resistance genes present in the corresponding host population.

§  Gene for gene interaction !!


Aggresiveness

§  aggressiveness: here, the ammount of spores produced per pustule by the rust pathogen.

§  Mechanism of gaining or loosing aggressiveness is not well investigated, but has nothing to do with the GFG interaction


Gene for gene (GFG) interaction

§  What is GfG

§  Individuum level §  Population level


Hypothesis:

-  Each host resistance à corresponding Avr gene

-  Avr alleles encode effector > plant detects effector and activates plant defences

-  Effector (protein or peptides) -  Recognition of Avr allele effectors

throgh receptor present in host plant cell > determination resistance or disease)

Figure: Prof Bruce A. McDonald Plant Pathology ETHZ

Materials and methods

§  Wild gene-for-gene interaction between Linum marginale and its host-specific rust pathogen Melamspora lini

§  Natural ecosystem: Kiandra plain (south Australia)

§  6 host populations and 6 pathogen populations were observed §  in the wild. §  And cross pollination in greenhouse.

§  Linum-Melamspore interaction: -  Genetic diversity of hosts and pathogens -  host resistance -  evolution of pathogen virulence and aggressiveness


Players


vs.

Linum marginale (Wilde Flax) Melamspsora lini (rust fungus)

§  M. lini - pathogen - §  Large production of uredospores §  Large dispersion (>100 km)

§  L. marginale - host - §  No specialized dispersal mechanisms “pepper-pot” §  tight inbreeders (Kiandra region) > exclusion of gene-flow through

pollen dispersal


Disease cicle during growing season

§  First infection §  Big production of new inoculi §  Quick transmission §  Leading to local epidemics


Results


suc res

vir avi

Results



Results


suc res

vir avi

Results


types in subsequent years, considerable vari-ability can be maintained for far longer thanin single populations. The effective host pop-ulation size for any given pathotype is a“moving target” that is at least partly deter-mined by the interaction of specific resistanceand virulence genes. This means that thethreshold for pathogen invasion will varyamong populations, among pathogen isolates,and even temporally within populations asresistance and virulence coevolve.

Although partial isolation among localpopulations can maintain high host andpathogen variability without assuming resis-tance or virulence costs (26), this does notexplain the failure of highly virulent patho-types to dominate the system. Our resultsindicate that a trade-off between virulence

and aggressiveness is likely to be a centralcausal factor in explaining these patterns.Indeed, further support for this idea comesfrom an earlier study where we comparedhost and pathogen variation in populations oftwo ecotypes of L. marginale occurring indistinctly different environments and varyingsignificantly in overall susceptibility (19). Asin the present study, the results showed thatpopulations of the more resistant ecotypewere dominated by more virulent M. linipathotypes. This suggests that although theunderlying resistance structure may havebeen generated by different mechanisms, theassociated pathogen populations have fol-lowed similar evolutionary trajectories in re-sponse to differences in the selective environ-ment generated by the hosts.

The strength of the positive relationshipbetween host resistance and pathogen viru-lence in the Linum-Melampsora interactionunderscores the potential for host variation todetermine evolutionary trajectories of patho-gen populations. Clearly, host populationsharboring many resistance alleles [often cor-related with average resistance (8, 19)] mayfavor the evolution of very different pathogenpopulations to those evolving in low diversityhost populations. Trade-offs between viru-lence and aggressiveness, such as shownhere, play a further important role in gener-ating local adaptation in gene-for-gene sys-tems by impeding the emergence and evolu-tion of highly virulent pathotypes capable ofattacking all host genotypes. This observationgoes to the heart of a major evolutionaryissue in plant and animal host-parasite sys-tems regarding the balance of selection favor-ing virulence versus aggressiveness, as wellas its implications for among-host diseasetransmission (25, 27, 28).

References and Notes1. A. V. Hill, Annu. Rev. Immunol. 16, 593 (1998).2. !!!! , Br. Med. Bull. 55, 401 (1999).3. K. J. Jeffery, C. R. Bangham, Microb. Infect. 2, 1335(2000).

4. L. Heyndrickx et al., AIDS 14, 1862 (2000).5. F. L. Black, G. Schiffman, J. P. Pandey, Exp. Clin.Immunogenet. 12, 206 (1995).

6. D. W. Coltman, J. G. Pilkington, J. A. Smith, J. M.Pemberton, Evolution 53, 1259 (1999).

7. S. Meagher, Evolution 53, 1318 (1999).8. P. H. Thrall, J. J. Burdon, Plant Pathol. 49, 767 (2000).9. C. M. Lively, Am. Nat. 153, S34 (1999).10. !!!! , J. Jokela, Evol. Ecol. Res. 4, 219 (2002).11. J. M. Musser, Emerg. Infect. Dis. 2, 1 (1996).12. C. R. Parrish, Vet. Microbiol. 69, 29 (1999).13. H. H. Flor, Adv. Genet. 8, 29 (1956).14. J. N. Thompson, J. J. Burdon, Nature 360, 121 (1992).15. J. J. Burdon, Evolution 48, 1564 (1994).16. !!!! , A. M. Jarosz, Plant Pathol. 41, 165 (1992).17. P. H. Thrall, R. Godfree, J. J. Burdon, Plant Pathol., inpress.

18. J. J. Burdon, P. H. Thrall, A. H. D. Brown, Evolution 53,704 (1999).

19. P. H. Thrall, J. J. Burdon, A. G. Young, J. Ecol. 89, 736(2001).

20. P. H. Thrall, J. J. Burdon, J. D. Bever, Evolution 56,1340 (2002).

21. S. Gandon, Ecol. Lett. 5, 246 (2002).22. !!!! , Y. Michalakis, J. Evol. Biol. 15, 451 (2002).23. Materials and methods are available as supportingmaterial on Science Online.

24. A. M. Jarosz, J. J. Burdon, Evolution 45, 1618 (1991).25. K. M. Chin, M. S. Wolfe, Plant Pathol. 33, 535 (1984).26. P. H. Thrall, J. J. Burdon, Plant Pathol. 51, 169 (2002).27. M. Lipsitch, E. A. Herre, M. A. Nowak, Evolution 49,743 (1995).

28. S. L. Messenger, I. J. Molineux, J. J. Bull, Proc. R. Soc.Lond. Ser. B 266, 397 (1999).

29. Earlier versions of this manuscript were read andgreatly improved by the comments of J. Antonovics,J. D. Bever, J. N. Thompson, E. A. Herre, and A. G.Young. We are grateful for the able technical assist-ance of C. Eliasson and L. Brown. This is the 16thpaper in a series documenting the L. marginale-M. linihost-pathogen system. P. H. Thrall acknowledges thesupport of a Queen Elizabeth II Fellowship.

Supporting Online Materialwww.sciencemag.org/cgi/content/full/299/5613/1735/DC1Materials and Methods

4 November 2002; accepted 27 January 2003

Fig. 3. Frequency of vir-ulent (A) and avirulent(K) pathotypes of M.lini in resistant (Kian-dra) and susceptible(P1) populations ofthe host plant L. margi-nale over six consecu-tive years. The two hostpopulations were 300m apart—the resistantpopulation was com-posed of at least 13 dif-ferent resistance pheno-types with!5% of indi-viduals fully susceptibleto a set of eight localpathotypes, whereas thesusceptible populationwas composed of twophenotypes with"80%of individuals susceptible to the same set of pathotypes. Pathotype K was capable of attacking only one hostline in a set of 11 differentially resistant lines, whereas pathotype A was able to attack four (this pathotypewas virulent on both resistance phenotypes present in P1, as well as all 13 phenotypes present in Kiandra).Asterisks denote the absence of a particular pathotype in a given year rather than missing data.

Fig. 4. Relationship be-tween the number of re-sistance genes over-come by individual M.lini isolates and their av-erage per-pustule sporeproduction (4 hemocy-tometer counts for eachof 10 pustules perpathogen isolate; 57 of60 pathogen isolateswere successful). Linearregressions showed sig-nificant negative rela-tionships between max-imum spore productionvalues and infectivity(r 2 # 0.99, P ! 0.001),and between the rangeof per-pustule sporeproduction values andinfectivity (r 2 # 0.69, P # 0.05), but no relationship between minimum spore production values andinfectivity, confirming the triangular relationship. Isolates from the two most susceptible L.marginale populations (SH1, WHP2) are represented by open circles, those from populationsshowing intermediate resistance (SH2, G1) by triangles, and isolates from the most resistantpopulations ( WHP1, G3) by filled circles.

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Results


marginale, several instances of recoloniza-tion over distances of 80 m or more wererecorded (17). In contrast, the seeds of Linummarginale have no specialized dispersalmechanisms, being distributed from opencapsules by a simple “pepper-pot” shakermechanism. Moreover, L. marginale popula-tions in the Kiandra region are known to betight inbreeders (18), thereby ruling out sig-nificant gene-flow through pollen dispersal.

Here we use the Linum-Melampsora inter-action (19, 20) to demonstrate the links amonggenetic diversity, host resistance, and the evo-lution of pathogen virulence and aggressiveness(defined here as pathogen fecundity—the num-ber of spores produced per pustule) in a naturalsystem. Previous work on a metapopulationoccurring on the Kiandra Plain, KosciuszkoNational Park, Australia, detected consider-able differentiation, within and among popu-lations, in resistance to local isolates of M.lini (19). Despite often marked differencesbetween closely adjacent host populations,there was clear evidence of a nonrandomspatial distribution of resistance, with nearbypopulations sharing more resistance pheno-types than more distant ones. Subsequentcross-inoculation studies demonstrated stronglocal adaptation by M. lini to its host popu-lations (20). This finding matched theoreticalexpectations for pathogens that disperse morebroadly than their hosts (21, 22).

Using the dataset generated for the localadaptation study, we have investigated therelationship between average host resistanceand average pathogen virulence in these samepopulations (23). The results indicate a verytight evolutionary link between the resistanceand virulence of associated host-pathogenpopulation pairs, such that the virulence of agiven pathogen population increases directlywith the mean resistance of plant populations(Fig. 1). However, given that susceptible andresistant host populations are often closelyadjacent in the Kiandra metapopulation (asclose as 300 m) and that pathogen popula-tions are highly variable and relatively mo-bile (16), this raises an important question:Why don’t highly virulent pathotypes domi-nate susceptible host populations (Fig. 2), asmight be expected from theory? This conun-drum is illustrated by clear evidence that overprolonged periods of time virulent pathotypesmay dominate highly diverse and resistanthost populations, whereas the same patho-types may be only intermittently present innearby susceptible populations [Fig. 3 (24)].

The most likely explanation for this ap-parent paradox is that aggressiveness (i.e.,greater spore production and transmission po-tential), mediated by among-pathotype com-petition, is favored over virulence in suscep-tible host populations, whereas the ability toinfect multiple host genotypes (greater viru-lence) is favored in resistant populations. Part

of this explanation rests on the assumption ofa negative relationship between virulence andaggressiveness (i.e., there is a cost to carryingextra virulence genes).

Using the set of M. lini isolates from thelocal adaptation study (20), we examined therelationship between spore production andthe number of L. marginale resistance genesthat a given pathogen isolate could over-come (23). The results show a triangularrelationship between average spore produc-tion and virulence such that pathotypes ableto overcome few resistance genes exhibit awide range of per pustule spore productionvalues, whereas more virulent pathotypesable to attack a greater proportion of resis-tance genes show reduced levels of sporeproduction (Fig. 4). Evidence for a trade-off between virulence and aggressivenesshas been found among different pathotypes

of Erysiphe graminis attacking mixtures ofthree differentially resistant barley lines(25). However, those results could not beset in an evolutionary context.

Although the most fit pathotypes in sus-ceptible populations are predicted to showhigh aggressiveness and low virulence (withthe converse for resistant host populations),less fit types may still be able to invadesusceptible host populations as long as theirrate of spread exceeds invasion thresholds.Although equilibrium predictions from singlepopulation models imply that the pathogenwith the highest reproductive rate (R0) willeventually come to dominate, this is not nec-essarily what will be observed in natural sit-uations. In wild host–pathogen metapopula-tions, where dynamics are highly stochasticwith frequent pathogen extinction followedby reinvasion by the same or different patho-

Fig. 1. Relationshipbetween mean plantpopulation resistance(fraction of pathogensagainst which resis-tance was observed)and mean virulence ofthe associated patho-gen populations (frac-tion of hosts whichcould be attacked).The best fit for the re-lationship was givenby a second-orderpower function (y ! ax [b " c ln(x)]), where xand y represent meanresistance and viru-lence, respectively [forcalculation of meanresistance and virulence values, see (22)].

Fig. 2. The fraction ofplants in each hostpopulation resistant toattack by the 10 iso-lates representing eachpathogen population.Pathogen populationsare arranged along thex axis in increasing or-der of average viru-lence from left to right.Within each pathogenpopulation, host popu-lations are arrangedfrom left to right in in-creasing order of aver-age resistance. Al-though glasshouse in-oculations showed thathighly virulent patho-gen populations (e.g.,G3) were able to infectnearly all the hosts en-countered in the metapopulation, these pathogens do not constitute a major proportion of thepathogens found in susceptible host populations (e.g., as indicated in the figure, pathogen populationSH1 shows low virulence against a majority of plants frommore resistant host populations). In fact, oneG3 isolate was able to infect all 120 plant lines across the six populations in greenhouse trials, yet thispathotype did not appear in any other population.

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types in subsequent years, considerable vari-ability can be maintained for far longer thanin single populations. The effective host pop-ulation size for any given pathotype is a“moving target” that is at least partly deter-mined by the interaction of specific resistanceand virulence genes. This means that thethreshold for pathogen invasion will varyamong populations, among pathogen isolates,and even temporally within populations asresistance and virulence coevolve.

Although partial isolation among localpopulations can maintain high host andpathogen variability without assuming resis-tance or virulence costs (26), this does notexplain the failure of highly virulent patho-types to dominate the system. Our resultsindicate that a trade-off between virulence

and aggressiveness is likely to be a centralcausal factor in explaining these patterns.Indeed, further support for this idea comesfrom an earlier study where we comparedhost and pathogen variation in populations oftwo ecotypes of L. marginale occurring indistinctly different environments and varyingsignificantly in overall susceptibility (19). Asin the present study, the results showed thatpopulations of the more resistant ecotypewere dominated by more virulent M. linipathotypes. This suggests that although theunderlying resistance structure may havebeen generated by different mechanisms, theassociated pathogen populations have fol-lowed similar evolutionary trajectories in re-sponse to differences in the selective environ-ment generated by the hosts.

The strength of the positive relationshipbetween host resistance and pathogen viru-lence in the Linum-Melampsora interactionunderscores the potential for host variation todetermine evolutionary trajectories of patho-gen populations. Clearly, host populationsharboring many resistance alleles [often cor-related with average resistance (8, 19)] mayfavor the evolution of very different pathogenpopulations to those evolving in low diversityhost populations. Trade-offs between viru-lence and aggressiveness, such as shownhere, play a further important role in gener-ating local adaptation in gene-for-gene sys-tems by impeding the emergence and evolu-tion of highly virulent pathotypes capable ofattacking all host genotypes. This observationgoes to the heart of a major evolutionaryissue in plant and animal host-parasite sys-tems regarding the balance of selection favor-ing virulence versus aggressiveness, as wellas its implications for among-host diseasetransmission (25, 27, 28).

References and Notes1. A. V. Hill, Annu. Rev. Immunol. 16, 593 (1998).2. !!!! , Br. Med. Bull. 55, 401 (1999).3. K. J. Jeffery, C. R. Bangham, Microb. Infect. 2, 1335(2000).

4. L. Heyndrickx et al., AIDS 14, 1862 (2000).5. F. L. Black, G. Schiffman, J. P. Pandey, Exp. Clin.Immunogenet. 12, 206 (1995).

6. D. W. Coltman, J. G. Pilkington, J. A. Smith, J. M.Pemberton, Evolution 53, 1259 (1999).

7. S. Meagher, Evolution 53, 1318 (1999).8. P. H. Thrall, J. J. Burdon, Plant Pathol. 49, 767 (2000).9. C. M. Lively, Am. Nat. 153, S34 (1999).10. !!!! , J. Jokela, Evol. Ecol. Res. 4, 219 (2002).11. J. M. Musser, Emerg. Infect. Dis. 2, 1 (1996).12. C. R. Parrish, Vet. Microbiol. 69, 29 (1999).13. H. H. Flor, Adv. Genet. 8, 29 (1956).14. J. N. Thompson, J. J. Burdon, Nature 360, 121 (1992).15. J. J. Burdon, Evolution 48, 1564 (1994).16. !!!! , A. M. Jarosz, Plant Pathol. 41, 165 (1992).17. P. H. Thrall, R. Godfree, J. J. Burdon, Plant Pathol., inpress.

18. J. J. Burdon, P. H. Thrall, A. H. D. Brown, Evolution 53,704 (1999).

19. P. H. Thrall, J. J. Burdon, A. G. Young, J. Ecol. 89, 736(2001).

20. P. H. Thrall, J. J. Burdon, J. D. Bever, Evolution 56,1340 (2002).

21. S. Gandon, Ecol. Lett. 5, 246 (2002).22. !!!! , Y. Michalakis, J. Evol. Biol. 15, 451 (2002).23. Materials and methods are available as supportingmaterial on Science Online.

24. A. M. Jarosz, J. J. Burdon, Evolution 45, 1618 (1991).25. K. M. Chin, M. S. Wolfe, Plant Pathol. 33, 535 (1984).26. P. H. Thrall, J. J. Burdon, Plant Pathol. 51, 169 (2002).27. M. Lipsitch, E. A. Herre, M. A. Nowak, Evolution 49,743 (1995).

28. S. L. Messenger, I. J. Molineux, J. J. Bull, Proc. R. Soc.Lond. Ser. B 266, 397 (1999).

29. Earlier versions of this manuscript were read andgreatly improved by the comments of J. Antonovics,J. D. Bever, J. N. Thompson, E. A. Herre, and A. G.Young. We are grateful for the able technical assist-ance of C. Eliasson and L. Brown. This is the 16thpaper in a series documenting the L. marginale-M. linihost-pathogen system. P. H. Thrall acknowledges thesupport of a Queen Elizabeth II Fellowship.

Supporting Online Materialwww.sciencemag.org/cgi/content/full/299/5613/1735/DC1Materials and Methods

4 November 2002; accepted 27 January 2003

Fig. 3. Frequency of vir-ulent (A) and avirulent(K) pathotypes of M.lini in resistant (Kian-dra) and susceptible(P1) populations ofthe host plant L. margi-nale over six consecu-tive years. The two hostpopulations were 300m apart—the resistantpopulation was com-posed of at least 13 dif-ferent resistance pheno-types with!5% of indi-viduals fully susceptibleto a set of eight localpathotypes, whereas thesusceptible populationwas composed of twophenotypes with"80%of individuals susceptible to the same set of pathotypes. Pathotype K was capable of attacking only one hostline in a set of 11 differentially resistant lines, whereas pathotype A was able to attack four (this pathotypewas virulent on both resistance phenotypes present in P1, as well as all 13 phenotypes present in Kiandra).Asterisks denote the absence of a particular pathotype in a given year rather than missing data.

Fig. 4. Relationship be-tween the number of re-sistance genes over-come by individual M.lini isolates and their av-erage per-pustule sporeproduction (4 hemocy-tometer counts for eachof 10 pustules perpathogen isolate; 57 of60 pathogen isolateswere successful). Linearregressions showed sig-nificant negative rela-tionships between max-imum spore productionvalues and infectivity(r 2 # 0.99, P ! 0.001),and between the rangeof per-pustule sporeproduction values andinfectivity (r 2 # 0.69, P # 0.05), but no relationship between minimum spore production values andinfectivity, confirming the triangular relationship. Isolates from the two most susceptible L.marginale populations (SH1, WHP2) are represented by open circles, those from populationsshowing intermediate resistance (SH2, G1) by triangles, and isolates from the most resistantpopulations ( WHP1, G3) by filled circles.

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Discussion

§  The pathogen populatons follow similar evolutionary pathways but in different selective environments.

§  There are two strategies: more agresssiveness or more virulence.

§  The highest reproduction rate (R0) is not always the best strategy.

§  High diverse host populations lead to high divers pathogen populations.


Discussion

§  Trade offs are important in the emerge of highly virulent

pathotypes that can attack all host genotypes

§  Threshold for pathogen invasion varies among populations.

§  In wild host-pathogen metapopulations dynamics are highly stochastic. There will always be a big genetic diversity of pathogens in this systems.


Selection on Erysiphe graminis in pure and mixed stands of barley K. M. Chin and M. S. Wolfe (1984)


https://www.uoguelph.ca/~gbarron/MISC2003/grassmic.htm

http://balespress.com/product/barley/

Introduction

§  Selection of the Erysiphe graminis in single and mixed cultivars of barley.

§  Experimental design: §  Pure stands and mixed stands with 2 (3) varieties of barley. §  Each barley cultivar had one resistant gene.


Frequence of pathogens


538 K.M. Chin and M.S. Wolfefrequencies of hwm, hw(m) and hm(w) werethen subtracted from 100 to give the frequencyQfh{w,m).

From the Test I infections on W and M.checks were again carried out on sets of 10single colony isolates to ensure that thegenotypes were being identified correctly.There were only occasional errors, whichcould have been due, for example, to inducedsusceptibility, but which made little differenceto the final calculations (Chin, 1979).

Quantitative variation in virulenceQuantitative variation in virulence amongisolates may arise in different ways duringcolony development, but they are integratedin the relative numbers uf survivors of eachisolate. Counting the number of actively sporu-lating colonies produced by different isolatesintegrates some, though not all of thesedifferences, and is a convenient and rapidmeasure.

To test for differences in quantitativevirulence of isolates with combined virulencefor Hassan and Wing, hw(m), tive singlecolonies were isolated from each of thesamples originally collected from H and Win pure stands and in the mixture H: W: M.The virulence (number of colonies formedper inoculated spore that germinated) ofeach isolate was assessed on leaf segments

of H and W. Spore germination was moni-tored on glass slides exposed near the ino-culated leaf segments in the settling tower(see also Chin era/., 1984).

RESULTS AND DISCUSSION

Mixture Trial 1977

Frequencies of pathogen genotypes withsimple and complex virulences on individualcultivarsIn pure stands, simple virulences (h(w) inH: H and w(hj in W; W) predominated inthe pathogen population (Table 3). Withincreasing dilution of Hassan in mixtures withWing, the frequency of/ivvon Hassan increasedmarkedly (Table 3a). For example, on Hassanin H;5W (1 part Hassan: 5 parts Wing) thefrequency of hw was 62-5% compared with15-5% in pure stands. Similarly, the frequencyof hw on Wing increased almost fourfold withincreasing dilution of Wing in mixtures withHassan (Table 3 b).

These results suggest that in pure stands,pathogen genotypes with simple virulenceswere more fit (i.e. left more survivors) tlianthose with more complex virulence. Inmixtures, whilst the fitness of each pathogengenotype remained the same on each cultivar,the mean fitnesses of the genotypes with

Table 3. Percentage distribution, in the 1977 trial, of pathogengenotypes with simple virulences h(wj and wfhj and complex viru-lence hw on (a) Hassan, grown as a pure stand (H : H) and in each ofthree mixtures, and on (b) Wing, grown as a pure stand (W : W) and

in each of three mixtures. Assessed at 67 days from sowing

Source of inoculum Mixture hw h(w) w(h)

(a) Hassan

L.S.I

(b) Wing

L.S.D.

H:HH:W

H:2WH:5W

15-523-738-862-5

(P = 0-05) 10-7(P=0-01) 17-7(P=0-001) 33-1

W:W 16-3W:H 38 4W:2H 48-8W:5H 60-6

(P = 0-05) 13-8(P = O-Ol) 25-4

84-576-361-237-5

83-761-651-239-4

Simple virulences complex virulences


Pure Stand (H:H)


H H

h(w)

hw

Mixture (H:W)


H

W

HW


Mixture (H:W)


HW HW

hw h(w)

Relative frequency


542 K. M. Chin and M. S. Wolfethe different pathogen genotypes over allcomponents in the mixture, the frequencieson each cultivar were first expressed in termsof the actual infection (colony number pertiller) present on that cultivar. The meanfrequency of each genotype was then calcu-lated by expressing the mean amount ofinfection caused by the genotype as a per-centage of mean infection in the mixture.Similarly, the mean frequency of each geno-type in pure stands was estimated from themean infection due to each genotype in allpure stands.

The data indicate increased selection forpathogen genotypes with the complex viru-lence wm(h} and hwm and possibly forhw(m), in the mixture compared to purestands (Table 5). There was however Uttle

from pure stands of Wing were more virulenton Wing than on Hassan. This differentialadaptation of complex isolates to their sourcecultivar (cultivar from which they wereisolated) is reflected in the significant (P<001)interaction effect between source and testcultivars. Comparison of the homologous andheterologous combinations* shows that as aresult of this adaptation, homologous com-binations have a mean virulence advantage of13-9 X 10~^ colonies per spore over hetero-logous combinations, equivalent to an increaseof 22-9%.

Isolates of hw(tn) obtained from Hassanand Wing in the mixture H; W; M did notshow differential adaptation; differencesbetween source cultivars, test cuhivars andinteraction effects between source and test

Table 5, Relative frequencies of pathogen genotypes with simple and complex virulences in pureand mixed stands of barley cultivars Hassan, Wing and Midas at 53 days from sowing

Simple virulencesh(w,m); \v(h,mj; mfh,wj

Complex virulenceshw(m): hm(w); wm(h) hwm

Mean of pure standsMean of mixture (H : W : M)

72-361-6

10-612-8

9-75-2

2-881

4-512-2

evidence to support the contention (e.g.Caldweli, 1968) that the use of mixed hostpopulations would result in rapid selectionof a 'super race' capable of attacking allcomponents in the mixture, because theabsolute frequencies (colonies per tiller) ofall genotypes, including those with complexvirulences, were reduced in the mixed standscompared to tbe means of the pure stands(Fig. 2). The increase in relative frequenciesof the tbree genotypes with complex virulenceswas more than offset by the overall reductionin population size of the pathogen in themixture.

Variation in the degree of virulence o/hw(m)isolatesDifferences in the degree of virulence ofhw(r}jjwere observed in isolates taken from cultivarsHassan and Wing in pure stands and in themixture H; W: M (Tables 6a, b).

Isolates of hwfm) taken from pure standsof Hassan were generally more virulent onHassan than on Wing, whereas tbose taken

50

4 0

30

20

10

DWean of pure standsH.H, W.W, M.M

0 Mean of all componentsof mixture H:W:M

m{h.,w) hmiw) hwmw{h,m) hw[m) wm{h)

Virulence combination

Fig. 2. Absolute frequencies of differentvirulence combinations (expressed as colonynumbers per tiller) in pure stands and inmixtures of Hassan, Wing, Midas, 53 daysfrom sowing.

Caten (1974); homologous, inoculationof cultivars with isolates obtained from these cultivars;heterologous, inoculation ol' cultivars with isolatesfrom other cultivais.

Absolute frequency


542 K. M. Chin and M. S. Wolfethe different pathogen genotypes over allcomponents in the mixture, the frequencieson each cultivar were first expressed in termsof the actual infection (colony number pertiller) present on that cultivar. The meanfrequency of each genotype was then calcu-lated by expressing the mean amount ofinfection caused by the genotype as a per-centage of mean infection in the mixture.Similarly, the mean frequency of each geno-type in pure stands was estimated from themean infection due to each genotype in allpure stands.

The data indicate increased selection forpathogen genotypes with the complex viru-lence wm(h} and hwm and possibly forhw(m), in the mixture compared to purestands (Table 5). There was however Uttle

from pure stands of Wing were more virulenton Wing than on Hassan. This differentialadaptation of complex isolates to their sourcecultivar (cultivar from which they wereisolated) is reflected in the significant (P<001)interaction effect between source and testcultivars. Comparison of the homologous andheterologous combinations* shows that as aresult of this adaptation, homologous com-binations have a mean virulence advantage of13-9 X 10~^ colonies per spore over hetero-logous combinations, equivalent to an increaseof 22-9%.

Isolates of hw(tn) obtained from Hassanand Wing in the mixture H; W; M did notshow differential adaptation; differencesbetween source cultivars, test cuhivars andinteraction effects between source and test

Table 5, Relative frequencies of pathogen genotypes with simple and complex virulences in pureand mixed stands of barley cultivars Hassan, Wing and Midas at 53 days from sowing

Simple virulencesh(w,m); \v(h,mj; mfh,wj

Complex virulenceshw(m): hm(w); wm(h) hwm

Mean of pure standsMean of mixture (H : W : M)

72-361-6

10-612-8

9-75-2

2-881

4-512-2

evidence to support the contention (e.g.Caldweli, 1968) that the use of mixed hostpopulations would result in rapid selectionof a 'super race' capable of attacking allcomponents in the mixture, because theabsolute frequencies (colonies per tiller) ofall genotypes, including those with complexvirulences, were reduced in the mixed standscompared to tbe means of the pure stands(Fig. 2). The increase in relative frequenciesof the tbree genotypes with complex virulenceswas more than offset by the overall reductionin population size of the pathogen in themixture.

Variation in the degree of virulence o/hw(m)isolatesDifferences in the degree of virulence ofhw(r}jjwere observed in isolates taken from cultivarsHassan and Wing in pure stands and in themixture H; W: M (Tables 6a, b).

Isolates of hwfm) taken from pure standsof Hassan were generally more virulent onHassan than on Wing, whereas tbose taken

50

4 0

30

20

10

DWean of pure standsH.H, W.W, M.M

0 Mean of all componentsof mixture H:W:M

m{h.,w) hmiw) hwmw{h,m) hw[m) wm{h)

Virulence combination

Fig. 2. Absolute frequencies of differentvirulence combinations (expressed as colonynumbers per tiller) in pure stands and inmixtures of Hassan, Wing, Midas, 53 daysfrom sowing.

Caten (1974); homologous, inoculationof cultivars with isolates obtained from these cultivars;heterologous, inoculation ol' cultivars with isolatesfrom other cultivais.

Lunedì, 16 novembre 15 26 D-USYS/Agrarwissenschaften/ Gioele Fiori, Christjohannes Gilli Lunedì, 16 novembre 15 26 D-USYS/Agrarwissenschaften/ Gioele Fiori, Christjohannes Gilli

Mixture (H:W)


Lunedì, 16 novembre 15 27 D-USYS/Agrarwissenschaften/ Gioele Fiori, Christjohannes Gilli Lunedì, 16 novembre 15 27 D-USYS/Agrarwissenschaften/ Gioele Fiori, Christjohannes Gilli

Reduction in absolute frequency


Conclusion

§  Complex form (hwm) has lower rate of reproduction and survival (trade off suggested)

§  Less absolute pathogen frequency in mixtures. §  Selection for pathogens with complex virulence may be

slow in mixed host populations. §  If the same host mixture is planted over years, very fit

complex pathogens adapted to this mixture could emerge.


evolution of virulence in plant host- pathogen metapopulation · evolution of virulence in plant...

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