Fitness Costs of Plant Disease Resistance

Brown, J. K. M.

doi:10.1002/9780470015902.a0020094

Cited by 4 publications

(5 citation statements)

References 32 publications

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“…This means that there was no full adaptation to Mla ‐based resistance in the pathogen population, indicating a long‐term evolutionary stability, in stark contrast to agricultural environments. This suggests that the evolutionary forces are very different in agricultural versus natural environments, where fitness costs of R genes might favour balancing evolution instead of selective sweeps (Brown, 2007).…”

Section: Discussionmentioning

confidence: 99%

The wheat Mla homologue TmMla1 exhibits an evolutionarily conserved function against powdery mildew in both wheat and barley

et al. 2011

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SUMMARYThe race-specific barley powdery mildew (Blumeria graminis f. sp. hordei) resistance gene Mla occurs as an allelic series and encodes CC-NB-LRR type resistance proteins. Inter-generic allele mining resulted in the isolation and characterisation of an Mla homologue from diploid wheat, designated TmMla1, which shares 78% identity with barley HvMLA1 at the protein level. TmMla1 was found to be a functional resistance gene against Blumeria graminis f. sp. tritici in wheat, hereby providing an example of R gene orthologs controlling the same disease in two different species. TmMLA1 exhibits race-specific resistance activity and its N-terminal coiled-coil domain interacts with the barley transcription factor HvWRKY1. Interestingly, TmMLA1 was not functional in barley transient assays. Replacement of the TmMLA1 LRR domain with that of HvMLA1 revealed that this fusion protein conferred resistance against B. graminis f. sp. hordei isolate K1 in barley. Thus, TmMLA1 not only confers resistance in wheat but possibly also in barley against an as yet unknown barley powdery mildew race. The conservation of functional R gene orthologs over at least 12 million years is surprising given the observed rapid breakdown of Mla-based resistance against barley mildew in agricultural ecosystems. This suggests a high stability of Mla resistance in the natural environment before domestication.

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Section: Discussionmentioning

confidence: 99%

The wheat Mla homologue TmMla1 exhibits an evolutionarily conserved function against powdery mildew in both wheat and barley

et al. 2011

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“…In a wide range of models, the frequency of RES at equilibrium is approximately equal to the cost of avr and the frequency of AVR is approximately proportional to the cost of RES (38,71,74,120). This is the result of negative feedback in the host-parasite interaction, so the ultimate effect of increasing the cost of avr is to increase the frequency of RES, leaving the frequency of avr unchanged, while increasing the cost of RES reduces the frequency of avr (Figure 3; see also 20,38).…”

Section: Costs Of Resistance and Virulencementioning

confidence: 96%

“…The cyclical dynamics of RES and avr frequencies depend on fitness costs causing those alleles to be removed from the population once they no longer benefit the host or parasite. Costs of resistance in plant disease have been reviewed elsewhere (14,18,20). Several types of cost have been attributed to RES genes involved in GFG interactions.…”

Section: Figurementioning

confidence: 99%

Plant-Parasite Coevolution: Bridging the Gap between Genetics and Ecology

Brown

Tellier²

2011

Annu. Rev. Phytopathol.

275

279

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We review current ideas about coevolution of plants and parasites, particularly processes that generate genetic diversity. Frequencies of host resistance and parasite virulence alleles that interact in gene-for-gene (GFG) relationships coevolve in the familiar boom-and-bust cycle, in which resistance is selected when virulence is rare, and virulence is selected when resistance is common. The cycle can result in stable polymorphism when diverse ecological and epidemiological factors cause negative direct frequency-dependent selection (ndFDS) on host resistance, parasite virulence, or both, such that the benefit of a trait to fitness declines as its frequency increases. Polymorphism can also be stabilized by overdominance, when heterozygous hosts have greater resistance than homozygotes to diverse pathogens. Genetic diversity can also persist in the form of statistical polymorphism, sustained by random processes acting on gene frequencies and population size. Stable polymorphism allows alleles to be long-lived and genetic variation to be detectable in natural populations. In agriculture, many of the factors promoting stability in host-parasite interactions have been lost, leading to arms races of host defenses and parasite effectors.

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“…Species are characterized by different fitness-related traits and strategies that were shaped by tradeoffs that constrain investment of resources in certain functions at the expense of others in the context of resource limitation [36,[78][79][80]. For example, investment in resistance to infection by parasites can be associated with a fitness cost and has been shown to vary according to host lifespan [36,37,81]. Across kingdoms, short-lived species (e.g.…”

Section: Host Ubiquity and Competence For Pathogen Spreadmentioning

confidence: 99%

Non-random biodiversity loss underlies predictable increases in viral disease prevalence

Lacroix

Jolles

Seabloom

et al. 2014

J. R. Soc. Interface.

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Disease dilution (reduced disease prevalence with increasing biodiversity) has been described for many different pathogens. Although the mechanisms causing this phenomenon remain unclear, the disassembly of communities to predictable subsets of species, which can be caused by changing climate, land use or invasive species, underlies one important hypothesis. In this case, infection prevalence could reflect the competence of the remaining hosts. To test this hypothesis, we measured local host species abundance and prevalence of four generalist aphid-vectored pathogens (barley and cereal yellow dwarf viruses) in a ubiquitous annual grass host at 10 sites spanning 2000 km along the North American West Coast. In laboratory and field trials, we measured viral infection as well as aphid fecundity and feeding preference on several host species. Virus prevalence increased as local host richness declined. Community disassembly was non-random: ubiquitous hosts dominating species-poor assemblages were among the most competent for vector production and virus transmission. This suggests that non-random biodiversity loss led to increased virus prevalence. Because diversity loss is occurring globally in response to anthropogenic changes, such work can inform medical, agricultural and veterinary disease research by providing insights into the dynamics of pathogens nested within a complex web of environmental forces.

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Fitness Costs of Plant Disease Resistance

Cited by 4 publications

References 32 publications

The wheat Mla homologue TmMla1 exhibits an evolutionarily conserved function against powdery mildew in both wheat and barley

The wheat Mla homologue TmMla1 exhibits an evolutionarily conserved function against powdery mildew in both wheat and barley

Plant-Parasite Coevolution: Bridging the Gap between Genetics and Ecology

Non-random biodiversity loss underlies predictable increases in viral disease prevalence

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