A model was adopted from Østergård & Hovmøller (1991)a and developed further to promote an understanding of the evolution of pathogen populations and the durability of disease resistance of crop cultivars as governed b y selection pressure exerted b y various types, sources and temporal deployment modes of host resistance, interplaying with virulence properties and aggressiveness of pathogen strains and the fitness costs associated with virulence features. The model addresses crop protection scientists, resistance breeders, extension workers, university teachers and their students, to stimulate ideas for deriving and testing hypotheses and concepts for sustainable disease resistance use and for exploring and developing resistance-based disease control scenarios and strategies that help to improve the durability of crop production systems, increase the market value of resistant varieties and the return on investment in resistance breeding, decrease disease-induced crop losses, protect genetic resources, reduce pesticide use in crop production and are compatible with organic farming practices.
The model of Østergård & Hovmøller (1991) depicts a system of three loci (x, y, z) of the haploid stage of a pathogen like powdery mildew on barley (Blumeria graminisf. sp. hordei), each with two alleles (A = avirulent, V = virulent) that interact with three loci of the corresponding major resistance (R) genes in the host (Rx, Ry and Rz, where the presence of an R gene confers resistance to the respective pathogen avirulence gene). The model could just as well be used to depict a system of three virulence factors (x, y, z) of the asexual stage of a pathogen, such as the dikaryotic uredo stage of wheat yellow rust (Puccinia striiformis f.sp. tritici, WYR), with each virulence factor conferring either avirulence (A) or virulence (V) to the corresponding R genes (Rx, Ry, Rz) in the host. Individual virulence/avirulence alleles and genotypes of the haploid mildew system would thus correspond to individual virulence/avirulence properties and phenotypes of the asexual dikaryotic rust system, respectively.
Frequency changes of virulence and avirulence alleles and genotypes (WYR asexual dikaryotic uredo stage: virulence and avirulence properties and phenotypes, respectively) of a pathogen population are computed by the model, as well as linkage disequilibria of alleles (WYR: linkage disequilibria of virulence / avirulence properties) and the mean relative fitness of the pathogen population over time. Following input data and parameters can be varied to explore the expected effects on pathogen populations: 1) the initial frequencies of individual pathogen genotypes (WYR: phenotypes), 2) the fractions of agricultural areas planted to host genotypes having particular disease resistance properties, 3) the resistance types (partial and/or complete) and sources (i. e. major genes for virulence-specific R and/or other genetic factors such as QTLs for virulence-non-specific R) possessed by individual crop cultivars, 4) the quantitative effects of R properties on pathogen fitness, 5) the fitness costs of individual virulence alleles (WYR: virulence properties) and 6) the relative aggressiveness of individual pathogen strains.
The model and some input data representing various scenarios for resistance gene deployment patterns and pathogen genotype (WYR: phenotype) frequencies in the initial pathogen population are on worksheets in an Excel file. Accompanying is a documentation and tutorial with step-wise exercises designed to explain how to use the model to design better strategies for durable resistance use, i.e. strategies that ensure low fitness of pathogen populations, combined with low selection pressure for virulence, - particularly multiple virulence -, resulting in low frequencies of virulent and, particularly, multiple-virulent pathogen genotyp es (WYR: phenotypes) as well as high proportions of multiple-avirulent pathogen genotypes (WYR: phenotypes) over time.
a Østergård, H. & Hovmøller, M. S., 1991: Gametic disequilibria between virulence genes in barley powdery mildew populations in relation to selection and recombination. I. Models. Plant Pathology 40:166-177.
Acknowledgement: This work was part of the RUSTFIGHT project funded b y the Danish Council for Strategic Research.