Innate Resistance

Abstract

It is common knowledge that each kind of organism has a relatively limited number of kinds of parasites that may be associated with it. Reciprocally, each kind of parasite has a more or less limited range of hosts, some parasites showing an exquisite specificity for one or very few host species. These properties clearly must be results of the different genetic characters of the organisms concerned. In plant pathology, where a great many different lines of both host plant and, for example, a fungal parasite are readily bred, all the data fit the so-called gene-for-gene hypothesis. This holds that a positive gene in the host plant and a corresponding positive gene in the fungal parasite produce incompatibility. Lack of either gene would permit the parasitic relationship. Furthermore, if one parasite/host gene pair specifies incompatibility, that gene pair will be epistatic to all parasite/host gene pairs that would permit a compatible relationship. If the genes Px of the parasite and Rx of the host determine an incompatible relationship, any mutation of Px to px resulting in loss of recognition of Rx should lead to a compatible relationship. Such mutations, i.e., to increased virulence, constitute loss of a specificity; they would be expected to occur readily and indeed they do. Mutation in the plant, however, from the susceptible state rx to Rx would be a gain of specificity. These would be expected to be rare, and they are.