Recognition and polymorphism in host—parasite genetics

Abstract

SUMMARYGenetic specificity occurs in many host-parasite systems. Each host can recognize and resist only a subset of parasites; each parasite can grow only on particular hosts. Biochemical recognition systems determine which matching host and parasite genotypes result in resistance or disease. Recognition systems are often associated with widespread genetic polymorphism in the host and parasite populations. I describe four systems with matching host-parasite polymorphisms: plant-pathogen interactions, nuclear-cytoplasmic conflict in plants, restriction enzymes in bacterial defence against viruses, and bacterial plasmids that compete by toxin production and toxin immunity. These systems highlight several inductive problems. For example, the observed patterns of resistance and susceptibility between samples of hosts and parasites are often used to study polymorphism. The detectable polymorphism by this method may be a poor guide to the actual polymorphism and to the underlying biochemistry of host-parasite recognition. The problem of using detectable polymorphism to infer the true nature of recognition and polymorphism is exacerbated by non-equilibrium fluctuations in allele frequencies that commonly occur in host-parasite systems. Another problem is that different matching systems may lead either to low frequencies of host resistance and common parasites, or to common resistance and rare parasites. Thus low levels of host resistance or rare parasites do not imply that parasitism is an unimportant evolutionary force on host diversity. Knowledge of biochemical recognition systems and dynamical analysis of models provide a framework for analysing the widespread polymorphisms in host-parasite genetics.

Statistical properties of polymorphism in host?parasite genetics

“…Matching specificity would lead to a high observed frequency of universal-susceptible alleles and universal host-range alleles. Alternatively, models that assumed some host alleles never matched parasites and some parasite alleles are never matched by hosts would also be consistent with the observations (Frank, 1993(Frank, , 1994. Thus, although Parker (1994) raised an interesting problem by showing that balanced polymorphisms are less conducive to sex than purely frequency-dependent polymorphisms, the data do not allow one to determine which model best describes plant-pathogen genetics.…”

Specific and Non-specific Defense against Parasitic Attack

“…But the biochemistry of the host}parasite interaction certainly must in#uence some of the key parameters, such as the number of matching speci"cities and the costs of resistance and virulence. Thus, full knowledge of population genetics and epidemiology depends on biochemical and mechanistic knowledge; likewise, the biochemistry and mechanisms of host}parasite interaction only have meaning when embedded within the dynamics of population genetics and epidemiology (Frank, 1994). This mutual dependence between the physical mechanisms of interaction and the population biology is further illustrated by the costs of resistance.…”

Genetic Variation Affecting Host–Parasite Interactions: Different Genes Affect Different Aspects of Sigma Virus Replication and Transmission in Drosophila melanogaster

“…Rather few studies have formally estimated how much genetic variation exists in natural populations for resistance to pathogens (Frank 1994;Bergelson et al 2001;Niare et al 2002). However, the existence of this genetic variation in disease resistance raises several key questions: How much genetic variation exists?, How many genes underlie this variation?, Which genes are responsible?, and How big are the effects of these genes?…”