The Evolutionary Genetics of Plant-Pathogen Systems

Simms, Ellen L.

doi:10.2307/1312816

Cited by 31 publications

(19 citation statements)

References 84 publications

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“…Disease resistance has been associated with a fitness "cost" (Crute, 1994;Bergelson and Purrington, 1996;Simms, 1996). In the (temporary) absence of pathogen pressure, individual plants with mutated R genes therefore may have selective advantages.…”

Section: Selective Pressures On Rpp5 Haplotypes and Gene Family Membersmentioning

confidence: 99%

“…In natural populations that are genetically and spatially more diverse, the evolutionary forces at work are less clear. However, the population dynamics of all plantpathogen systems are strongly influenced by genetic variation in resistance and virulence determinants (Crute, 1994;Simms, 1996). Parallels have been proposed between the evolution of plant R genes and of genes in the major histocompatibility complex (MHC) of vertebrates (Dangl, 1992;Michelmore and Meyers, 1998).…”

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confidence: 99%

“…If so, one of these Col-0 homologs could be the Col-0 RPP4 gene that recognizes the P. parasitica strain Emoy2 (Tör et al, 1994). Apparently, nonfunctional R gene homologs also might serve a repository function and allow mutation, unequal recombination, and gene conversion to generate novel R gene variants upon which diversifying selection can operate.Disease resistance has been associated with a fitness "cost" (Crute, 1994;Bergelson and Purrington, 1996;Simms, 1996). In the (temporary) absence of pathogen pressure, individual plants with mutated R genes therefore may have selective advantages.…”

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confidence: 99%

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Pronounced Intraspecific Haplotype Divergence at the RPP5 Complex Disease Resistance Locus of Arabidopsis

Noël¹,

Moores²,

Biezen³

et al. 1999

The Plant Cell

117

203

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In Arabidopsis ecotype Landsberg erecta (L er ), RPP5 confers resistance to the pathogen Peronospora parasitica. RPP5 is part of a clustered multigene family encoding nucleotide binding-leucine-rich repeat (LRR) proteins. We compared 95 kb of DNA sequence carrying the L er RPP5 haplotype with the corresponding 90 kb of Arabidopsis ecotype Columbia (Col-0). Relative to the remainder of the genome, the L er and Col-0 RPP5 haplotypes exhibit remarkable intraspecific polymorphism. The RPP5 gene family probably evolved by extensive recombination between LRRs from an RPP5 -like progenitor that carried only eight LRRs. Most members have variable LRR configurations and encode different numbers of LRRs. Although many members carry retroelement insertions or frameshift mutations, codon usage analysis suggests that regions of the genes have been subject to purifying or diversifying selection, indicating that these genes were, or are, functional. The RPP5 haplotypes thus carry dynamic gene clusters with the potential to adapt rapidly to novel pathogen variants by gene duplication and modification of recognition capacity. We propose that the extremely high level of polymorphism at this complex resistance locus is maintained by frequency-dependent selection. INTRODUCTIONPlant resistance to animal, fungal, bacterial, and viral pathogens often is governed by gene-for-gene interactions between host resistance ( R ) genes and corresponding pathogen avirulence ( Avr ) genes (Crute, 1994). In the absence of matching R genes, Avr gene products presumably enhance pathogen virulence (Collmer, 1998). Different pathogen strains carry different arrays of Avr genes (e.g., Holub and Beynon, 1996), which may indicate some functional redundancy. In crop monocultures, R genes impose strong selection on pathogen Avr genes for mutations to virulence; as a consequence, plant breeders must continuously recruit new R genes from wild relatives. In natural populations that are genetically and spatially more diverse, the evolutionary forces at work are less clear. However, the population dynamics of all plantpathogen systems are strongly influenced by genetic variation in resistance and virulence determinants (Crute, 1994;Simms, 1996). Parallels have been proposed between the evolution of plant R genes and of genes in the major histocompatibility complex (MHC) of vertebrates (Dangl, 1992;Michelmore and Meyers, 1998). It is of major interest, therefore, to understand the molecular basis for the evolution of host-pathogen specificity and to characterize intraspecific natural variation at R gene haplotypes. Interspecific comparisons have been reported elsewhere Thomas et al., 1998).The capacity to adapt rapidly to a broad spectrum of novel pathogen variants imposes a need for a mechanism that generates new R gene alleles. Many R genes are members of gene families residing at complex loci that can carry several distinct pathogen recognition specificities (HammondKosack and Jones, 1997). R genes, therefore, probably evolve novel Avr recognition capacities...

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Section: Selective Pressures On Rpp5 Haplotypes and Gene Family Membersmentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Pronounced Intraspecific Haplotype Divergence at the RPP5 Complex Disease Resistance Locus of Arabidopsis

Noël¹,

Moores²,

Biezen³

et al. 1999

The Plant Cell

117

203

View full text Add to dashboard Cite

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“…Most of what we know about the evolution of plant resistance to pathogens comes from studies of agricultural species or their wild relatives that address race specific, qualitative, gene-for-gene resistance mechanisms (Flor, 1971;Burdon, 1987;Simms, 1996 ). In these systems, host genotypes are either resistant to a specific pathogen race because they can recognize and eliminate it via the hypersensitive response, or susceptible because the pathogen is not recognized until after the disease is established, if at all (Staskawicz et al ., 1995).…”

Section: Introductionmentioning

confidence: 99%

Genotype, environment, and genotype by environment interactions determine quantitative resistance to leaf rust (Coleosporium asterum) in Euthamia graminifolia (Asteraceae)

2004

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Summary• The strength and consistency of genotypic differences in disease resistance determine the potential for resistance evolution in host populations that rely on vegetative reproduction. Here we surveyed infection intensity of host genotypes across space and time to estimate genotypic and environmental effects on quantitative disease resistance.• Cloned fragments of 12 Euthamia graminifolia genotypes were grown in unweeded experimental fields and outdoor pots. Infection intensity was surveyed during 2 yr of natural infection by the non-systemic rust pathogen, Coleosporium asterum .• Five of six surveys detected infection intensity differences among genotypes, despite substantial variation in mean infection intensity across surveys. When resistance was defined relative to local pathogen density, 10 -40% of resistance variation was due to host genotype. Although two genotypes exhibited greater resistance across environments, G × E interactions in resistance were common. Furthermore, infection intensity was unrelated to host size.• We conclude that quantitative resistance level can evolve in this system and show how logistic analysis (relative to local pathogen density) can provide insight into the mechanism(s) responsible for G × E interactions in infection intensity.

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“…Such a level of extensive variations indicates that the level of genetic variance in host resistance and pathogen virulence can strongly influence the population dynamics and equilibrium of the interacting species. The earlier studies on various host-pathogen systems [21], including Alternaria-Brassica, are restricted to single Alternaria species, with limited host differentials [2,5,6,10].…”

Section: Discussionmentioning

confidence: 99%

Evaluation of Pathological Variations in Alternaria Species Infecting Oilseed Brassicas in Diverse Regions of India for Induction of Systemic Resistance

Agnihotri¹

2016

JBMOA

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Isolation and purification of fungal culturesSamples of Alternaria blight infected leaves from various Brassica species were collected/procured from Northern and North-western regions of India. The fungal cultures were isolated and purified on PDA (potato dextrose agar) medium under AbstractThe 32 isolates of A. brassicae, 20 isolates of A. brassicicola and 3 isolates of A. alternata originating from diverse regions of North-West India, where Alternaria blight is highly prevalent, were investigated for their pathogenicity on various host species. The disease reaction varied with necrotic lesions of 0.4-7.5mm, mostly having brown to black coloured lesions. The isolates caused moderate to severe chlorosis on B. rapa varieties (YSH-401 and Pusa gold) as compared to the B. juncea varieties (Varuna, Rohini, Kranti and PHR-01). The mean disease index varied from 2.22 ± 1.17 to 7.32 ± 0.67 in A. brassicae isolates, 2.38 ± 0.92 to 5.89 ± 0.89 in A. brassicicola isolates and 2.49 ± 0.97 to 5.87 ± 0.91 in A. alternata isolates. Out of seven A. brassicae isolates that tested positive for non-aggressiveness on specific host species, five isolates, on prior inoculation, induced tolerance to highly aggressive strains of A. brassicae in the respective B. juncea and B. rapa varieties. The study thus opens up the possibility of deploying attenuated virulence as naturally occurring biological control for induction of systemic resistance/tolerance in Brassicas against A. brassicae, one of the most destructive fungal pathogen.

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The Evolutionary Genetics of Plant-Pathogen Systems

Cited by 31 publications

References 84 publications

Pronounced Intraspecific Haplotype Divergence at the RPP5 Complex Disease Resistance Locus of Arabidopsis

Pronounced Intraspecific Haplotype Divergence at the RPP5 Complex Disease Resistance Locus of Arabidopsis

Genotype, environment, and genotype by environment interactions determine quantitative resistance to leaf rust (Coleosporium asterum) in Euthamia graminifolia (Asteraceae)

Evaluation of Pathological Variations in Alternaria Species Infecting Oilseed Brassicas in Diverse Regions of India for Induction of Systemic Resistance

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