Abstract

Genotypic trade‐offs are fundamental to the understanding of the evolution of life‐history traits. In particular, the evolution of optimal host defense and the maintenance of variation in defense against infectious disease is thought to be underpinned by such evolutionary trade‐offs. However, empirical demonstrations of these trade‐offs that satisfy the strict assumptions made by theoretical models are rare. Additionally, none of these trade‐offs have yet been shown to be robustly replicable using a variety of different experimental approaches to rule out confounding issues with particular experimental designs. Here, we use inbred isolines as a novel experimental approach to test whether a trade‐off between viral resistance and growth rate in Plodia interpunctella, previously demonstrated by multiple selection experiments, is robust and meets the strict criteria required to underpin theoretical work in this field. Critically, we demonstrate that this trade‐off is both genetic and constitutive. This finding helps support the large body of theory that relies on these assumptions, and makes this trade‐off for resistance unique in being replicated through multiple experimental approaches and definitively shown to be genetic and constitutive.

Highlights

  • Genotypic trade-offs are fundamental to the understanding of the evolution of life-history traits

  • We use inbred isolines as a novel experimental approach to test whether a trade-off between viral resistance and growth rate in Plodia interpunctella, previously demonstrated by multiple selection experiments, is robust and meets the strict criteria required to underpin theoretical work in this field

  • The understanding of trade-offs remains central to evolutionary ecology (Shoval et al 2012; Acerenza 2016)

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Summary

Introduction

Genotypic trade-offs are fundamental to the understanding of the evolution of life-history traits. The understanding of trade-offs remains central to evolutionary ecology (Shoval et al 2012; Acerenza 2016) They are fundamental to understanding life histories in general (Roff and Fairbairn 2007), and in the context of the evolution of infectious disease, trade-offs are generally assumed to determine both the evolution of pathogen virulence (May and Anderson 1983; Alizon et al 2009; Alizon and Michalakis 2015), and host resistance to pathogens (Gillespie 1975; Sheldon and Verhulst 1996; Gemmill and Read 1998; Boots and Haraguchi 1999).

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