Submitted to: Book Chapter
Publication Type: Book / Chapter
Publication Acceptance Date: 7/17/1996
Publication Date: N/A
Citation: N/A Interpretive Summary: Most resistance against rust and mildew diseases in cereal crops is race specific. A resistance gene may provide complete protection against many pathogen races but no resistance at all against other races. Plant breeders choose resistance genes that are most effective against races present where the crop will be grown. This works well until new races appear that are not controlled by those resistance genes. Sometimes new races appear within only a few years. Resistance genes in our crops came originally from wild relatives of crops, so we set out to learn more about how the wild plant species coexist with their pathogens. We studied how resistance in wild plants changes in response to pathogen races and how pathogen races change in response to new types of resistance. We compared data from diseases of wild plants with predictions from computer simulated plant and pathogen interactions. The computer model yielded patterns of resistance and virulence that resemble patterns found in diseases of wild plants. In the computer model, as in nature, populations of plants and their pathogens came to an equilibrium with stable levels of resistance and virulence. Insights gained from the model will be useful for identifying the best places to find new resistance genes in wild relatives of crop plants and in selecting types of resistance that will be least liable to succumb to new races of the pathogen. This kind of information is needed especially for cereal crops, but is also needed in breeding for disease resistance in vegetables and fruits as well as other field crops.
Technical Abstract: Evidence from natural host-pathogen systems is consistent with expectations for balanced rather than transient polymorphisms of resistance and virulence in gene-for-gene interactions. Simulations with a population genetics model for gene-for-gene interactions showed that balanced polymorphisms require a fitness cost of virulence. Equilibria are more stable if the fitness cost applies only to unnecessary virulence on susceptible hosts rather than to a reduction in intrinsic growth rate on all hosts. When equilibria in the model are stable, the approach to equilibrium may take thousands of host generations for single isolated host and pathogen populations, but sub-populations of host and pathogen in patchy environments come to equilibrium within a few hundred generations if there is some pathogen gene flow between patches. When disease severity differs for different patches of host sub-populations, the phenotype frequencies oscillate out of phase in different patches, so pathogen gene flow between patches causes strong damping of the oscillations. Loss of resistance by one host sub-population in the model increases the stability of polymorphisms in the other sub-populations. Thus, the simple population genetics model can account for highly stable polymorphisms at the meta-population level for gene-for-gene interactions in natural host-pathogen systems.