Abstract

Fitness costs associated with resistance or virulence genes are thought to play a key role in determining the dynamics of gene-for-gene (GFG) host-parasite coevolution. However, the nature of interactions between fitness effects of multiple resistance or virulence genes (epistasis) has received less attention. To examine effects of the functional form of epistasis on the dynamics of GFG host-parasite coevolution we modified a classic multilocus GFG model framework. We show that the type of epistasis between virulence genes largely determines coevolutionary dynamics, and that coevolutionary fluctuations are more likely with acceleratingly costly (negative) than with linear or deceleratingly costly (positive) epistasis. Our results demonstrate that the specific forms of interaction between multiple resistance or virulence genes are a crucial determinant of host-parasite coevolutionary dynamics.

Highlights

  • Parasites are ubiquitous in biological systems, and the coevolutionary arms races between hosts and their parasites are thought to drive a wide range of ecological and evolutionary phenomena [1]

  • One of the primary frameworks developed to study host-parasite coevolutionary dynamics is the gene-for-gene (GFG) model, which emerged from empirical studies on plant-pathogen dynamics [2,3]

  • The dynamic interactions between hosts and parasites result in an escalatory arms race, with increases in the frequencies of resistant and virulent alleles

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Summary

Introduction

Parasites are ubiquitous in biological systems, and the coevolutionary arms races between hosts and their parasites are thought to drive a wide range of ecological and evolutionary phenomena [1]. The dynamic interactions between hosts and parasites result in an escalatory arms race, with increases in the frequencies of resistant and virulent alleles. A fundamental assumption of multilocus GFG models that has not previously been examined is the nature of the costs associated with host resistance or parasite virulence and how their fitness effects interact (i.e., the functional form of epistasis).

Results
Conclusion

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