Abstract

The pathogen Ustilago bullata often causes epidemic levels of head smut disease in Intermountain populations of the inbreeding annual grass Bromus tectorum. We examined patterns of genetic variation for virulence and for amplified fragment length polymorphism (AFLP) markers in four U. bullata populations on B. tectorum in northern Utah and southern Nevada. Patterns of disease incidence generally supported a gene‐for‐gene model for virulence and resistance in this pathosystem. Most host lines were susceptible to most or all paired isolates included in cross‐inoculation tests, but we found evidence for the existence of four avirulence genes. Host lines with alleles conferring resistance were usually resistant to races not found in co‐occurring pathogen populations. The exception was the population at Potosi Pass, Nevada, where the prevalent host line possessed an allele conferring resistance to one of two co‐occurring races. The two pathogen races at Potosi Pass were also strongly genetically differentiated in terms of their AFLP genotypes, whereas for the other three populations, there was no relationship between virulence phenotype and AFLP genotype. There was little evidence for high levels of inbreeding in the northern pathogen populations, which showed no clear groupings of isolates within or among populations. The correlation of the virulence phenotype with the AFLP genotype at Potosi Pass was associated with the presence of a mating locus–linked haplolethal trait in the race pathogenic on the prevalent host line. The presence of this trait is coincident with a high level of intratetrad selfing in this race, thus isolating it from the co‐occurring race and leading to fixation of most AFLP markers. The Potosi Pass population was also clearly differentiated from the northern populations, which were genetically similar to each other, a pattern also seen in the co‐occurring host populations, providing evidence for the idea of pathogen dispersal through seedborne inoculum.

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