where each pathogen strain is inoculated onto a defined host genotype in the same environment, allowing quantification of a range of different parameters (Table 2.2). Change in the aggressiveness of a pathogen is sometimes an important factor in the emergence of new invasive strains or increases in the severity of disease epidemics. For instance, the recent spread of yellow rust (Puccinia striiformis) to new regions has been linked to the appearance of strains with a more rapid disease cycle, greater production of spores, and the ability to cause epidemics under warmer conditions than those favored by previous strains.
Table 2.2 Some parameters used to measure aggressiveness
| Length of latent period (time from inoculation to production of new inoculum) |
| Rate of multiplication of the pathogen in host tissues (used for bacteria and viruses) |
| Rate of lesion expansion |
| Number of lesions produced per amount of initial inoculum |
| Eventual lesion size or extent of host tissue infected |
| Number of spores or cells produced per unit area of host tissue |
Genetic Control of Resistance and Virulence
In common with all other biological characteristics, host resistance and pathogen virulence are genetically determined. However, these two properties can only be assessed in the presence of the other partner. In the majority of cases, host resistance or pathogen virulence are not obviously correlated with other phenotypic characters. Features of the pathogen, such as rapid and extensive growth or the production of cell wall‐degrading enzymes, may or may not be related to virulence. Assessments of resistance and virulence are therefore based on disease reaction types. An interaction where symptoms are clearly expressed is described as a compatible disease reaction as opposed to an incompatible reaction where symptoms do not develop and the effect on the plant is minimal (Figure 2.6).
Host resistance is controlled by one or a few genes whose individual effects may be easily detected, or by a multiplicity of genes, each of which contributes only a small fraction of the property as a whole. The practical implications of this are described in more detail in Chapter 12. In a few instances, disease reaction type has been shown to be controlled by factors inherited through the host's cytoplasm. The best‐known example of such cytoplasmic inheritance involves the reaction of maize to the leaf blight fungus Bipolaris maydis. In the past, the production of hybrid maize has involved the laborious task of detasselling by hand to avoid self‐pollination occurring. The discovery of a cytoplasmically inherited mitochondrial factor for male sterility (Cms), which meant that cross‐pollination was essential, removed the need for this operation. Because of this, cultivars possessing Cms came to predominate throughout the USA. Unfortunately, Cms was also correlated with susceptibility to a particular strain (race T) of B. maydis. As a result, the occurrence in 1970 of favorable conditions for the development of the pathogen resulted in a disastrous epidemic (see Chapter 5, Figure 5.1). In any breeding program, the possibility that the cytoplasm may be important in disease resistance must therefore be considered.
Although pathogen virulence, host resistance, and disease reaction types are genetically determined, the environment may modify the expression of any of these characters. For example, the Sr6 gene conferring resistance in wheat to black stem rust is effective at 20 °C, but is inoperative at 25 °C.
Gene‐for‐Gene Theory
From an evolutionary viewpoint, it is predictable that genetic systems determining virulence in the pathogen will be paralleled by genes conferring resistance in the host. This is because any mutation to virulence in a pathogen population will be countered by the selection of hosts able to resist this more aggressive pathogen. Evolutionary biologists describe such a dynamic process of complementary changes as an “arms race.” Thus, in an ideal world we might envisage a perpetual stalemate, with host and pathogen populations being closely matched in resistance and virulence. Hence over a period of several years disease would be neither completely absent nor would it become rampant.
Support for these ideas has been obtained by field observations and experimental studies on several plant pathosystems. The planting of crop cultivars containing a limited number of specific resistance genes will tend to select for pathogen strains possessing complementary virulence. Strains of a pathogen which differ in specific virulence genes are usually called races. The races present in any one season or in a particular locality may be identified by their behavior on a selection of cultivars carrying different combinations of genes conferring resistance. A hypothetical interaction between several races of a pathogen and a differential set of host cultivars is shown in Table 2.3.
Further analysis of such differential interactions has shown that there is a precise genetic relationship between the two partners. The pioneering study was done by Harold Flor, who analyzed the genetics of host resistance and pathogen virulence using flax rust, Melampsora lini, as a model. Flor showed that for each host gene conferring resistance, there is a complementary gene in the pathogen determining virulence. This finding has become widely known as the gene‐for‐gene theory of host–pathogen interactions. On the basis of Flor's theory, the possible interactions between a pair of alleles governing resistance in a plant and the corresponding pair determining virulence in the pathogen can be shown as a quadratic check (Figure 2.7). In this scheme, a resistant reaction occurs only where an allele for resistance in the host plant interacts with an allele for avirulence in the pathogen.
Table 2.3 Hypothetical interaction between four host cultivars and four pathogen races
| Host | Pathogen | |||
| Race 1 | Race 2 | Race 3 | Race 4 | |
| Cultivar 1 | + | − | − | − |
| Cultivar 2 | − | + | − | − |
| Cultivar 3 | − | − | + | − |
| Cultivar 4 | − | − | − | + |
+ = compatible disease reaction (host susceptible, pathogen virulent).
− = incompatible disease reaction (host resistant, pathogen avirulent).
