Plant breeders have identified resistance alleles in wild plant isolates and have exploited these alleles in breeding modern, disease-resistant cultivars. Insight into the genetic basis of resistance and susceptibility in plants may provide models for the establishment of human diseases. We have chosen to study the powdery mildew disease of barley, caused by the obligate ascomycete, Erysiphe graminis f. sp. hordei. Barley - E. graminis interactions are characterized by extreme specificity. That is a given barley line is resistant to a specific set of E. graminis races, and conversely a given race is virulent on a limited, specific set of barley lines. A widely accepted hypothesis in the plant pathology literature, the """"""""gene- for-gene"""""""" hypothesis, suggests that the minimum number of genes which distinguish resistance from susceptibility is one. Our preliminary data suggest that the """"""""gene-for-gene"""""""" hypothesis does not adequately describe race-specific resistance to E. graminis in barley. In the present study the number of genes conditioning resistance to a specific E. graminis race will be determined by mutational analysis. We shall screen a mutagenized population of resistant barley seedlings for susceptible mutants. Detailed cytological analysis of the infection sequence of susceptible barley mutants will provide information about the contribution of each disease reaction gene to the establishment of incompatible relationships and the expression of resistance. Once the genetic basis of resistance is adequately understood strategies for cloning resistance genes can be devised. As a consequence of such knowledge more rational approaches to the development of resistant barley cultivars using variability in disease resistance extant in wild isolates, and in the future, variability generated by in vitro manipulation of cloned disease reaction genes may be undertaken.
