Mutants of Fusarium oxysporum f. sp. lycopersiei were obtained by UV irradiation. The mutants of race 1 and race 2 caused disease symptoms on plants with resistance genes against the corresponding wild type strains. Mutants of race 1 of the pathogen were stable, whereas mutants of race 2 lost the ability to cause disease symptoms in plants carrying the 1-2 resistance gene, after prolonged maintenance on potato dextrose agar. Mutants of race 1 resembled race 2 in pathogenicity and they were vegetatively compatible with race 2, but no longer with race 1. These results suggest that the iso]ated strains with ah altered virulence pattern have mutations in loci involved in avirulence.
IntroduetionPopu[ations of Fusarium oxysporum Schlecht. are differentiated in formae speciales and races based on differences in pathogenicity to various hosts and specificity to cultivars of the host. Race-cultivar specificity of many plant-pathogen interactions can be described by a gene-for-gene model (Crute, 1985). This model impIies that a product of an avirulence gene of the pathogen is recognized by a product of a resistance gene of the plant, resulting in ah incompatible interaction. Races of a pathogen without a functional avirulence gene cause a susceptible reaction, because they are not recognized by the host.In Fusarium wilt of tomato caused by E oxysporum f. sp. lycopersici a gene-forgene relation could exist. The resistance of the plant is controlled by dominant genes: the I-1 gene against race 1 of the fungus and the I-2 gene against race 2. Because classical genetic studies are not possible with this anamorphic fungus, the molecular basis of virulence and avirulence is difficult to investigate.Induction of mutations from avirulence to virulence can give evidence for the existence of a gene-for-gene relation in this plant-pathogen interaction. Such mutations from avirulence to virulence have been reported for several plant pathogens.