Abstract
BackgroundThe antagonistic co-evolution of hosts and their parasites is considered to be a potential driving force in maintaining host genetic variation including sexual reproduction and recombination. The examination of this hypothesis calls for information about the genetic basis of host-parasite interactions – such as how many genes are involved, how big an effect these genes have and whether there is epistasis between loci. We here examine the genetic architecture of quantitative resistance in animal and plant hosts by concatenating published studies that have identified quantitative trait loci (QTL) for host resistance in animals and plants.ResultsCollectively, these studies show that host resistance is affected by few loci. We particularly show that additional epistatic interactions, especially between loci on different chromosomes, explain a majority of the effects. Furthermore, we find that when experiments are repeated using different host or parasite genotypes under otherwise identical conditions, the underlying genetic architecture of host resistance can vary dramatically – that is, involves different QTLs and epistatic interactions. QTLs and epistatic loci vary much less when host and parasite types remain the same but experiments are repeated in different environments.ConclusionThis pattern of variability of the genetic architecture is predicted by strong interactions between genotypes and corroborates the prevalence of varying host-parasite combinations over varying environmental conditions. Moreover, epistasis is a major determinant of phenotypic variance for host resistance. Because epistasis seems to occur predominantly between, rather than within, chromosomes, segregation and chromosome number rather than recombination via cross-over should be the major elements affecting adaptive change in host resistance.
Highlights
The antagonistic co-evolution of hosts and their parasites is considered to be a potential driving force in maintaining host genetic variation including sexual reproduction and recombination
[5], and the improvement of resistance by genetic engineering [6]. These observations demonstrate the genetic basis of an interaction between host and parasite, typically they are silent about how the respective genes are arranged on the genome and whether and how they interact – they tell us little about the "genetic architecture" of loci involved in the interaction with parasites
[10], all experiments included a search for additive quantitative trait loci (QTL); epistatic interactions between these additive loci were examined in 86 experiments, with a further 62 cases in which the whole genome was scanned for epistatic interactions (Table 3)
Summary
The antagonistic co-evolution of hosts and their parasites is considered to be a potential driving force in maintaining host genetic variation including sexual reproduction and recombination. The interaction of hosts with their parasites is strongly affected by genotype [1] as shown, for example, by the interactions between host and parasite genotypes [2], the potential for increased parasite resistance by artificial selection [3], the direct identification of single genes [4], the molecular signature of selection in wild populations [5], and the improvement of resistance by genetic engineering [6] These observations demonstrate the genetic basis of an interaction between host and parasite, typically they are silent about how the respective genes are arranged on the genome and whether and how they interact – they tell us little about the "genetic architecture" of loci involved in the interaction with parasites. The genetic architecture of traits is of considerable interest as it affects host-parasite evolutionary interactions in many – albeit not fully understood – ways
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