The adaptive potential of clonality in aphid crop pests

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Aphids are among the world's most damaging group of insect pests, causing billions of US dollars of yield loss per annum to a wide range of food and commodity crops. The control of pest aphids has relied heavily on the use of chemical insecticides, however, the evolution of resistance poses a growing threat to their sustainable control.Aphids are in part so successful because of their remarkable capacity to rapidly increase in number under favourable conditions, indeed, it has been estimated that without predation or disease a single aphid could produce 600 billion descendants in just one season. This incredible reproductive output is achieved by asexual reproduction (parthenogenesis) - with adult female aphids giving birth to daughters that are clones of themselves for most of the growing season. For most aphid species this mode of reproduction alternates with a yearly cycle of sexual reproduction, however, in some countries such as the UK certain species, including important pests such as Myzus persicae, reproduce exclusively by parthenogenesis.Because aphid clonal lineages have been assumed to be genetically identical they have been referred to as 'evolutionary dead ends' with little or no capacity to evolve. However, we have recently shown that aphid clonal populations derived from a single female aphid can evolve heritable resistance to insecticides. Although this clearly demonstrates that aphid clonal lineages have adaptive potential the mechanisms by which aphid clones evolve are completely unknown. The aim of this project is to understand the adaptive potential of aphid clonal lineages and the molecular mechanisms underpinning clonal evolution in aphids. We will use the global aphid pest M. persicae as a model and exploit recent advances in genomics, transcriptomics and epigenetics to address a range of key knowledge gaps on this topic. These include understanding how quickly mutations accumulate in aphid clonal lineages, how this is affected by pesticide stress, and how clones adapt at the phenotypic and molecular level in the absence of sex. In the first objective of the proposal we will calculate the frequency and spectrum of mutations that spontaneously arise in clones of M. persicae using an experimental approach called mutation accumulation (which overcomes the difficulty of directly studying how rare mutations arise by allowing them to build up over several generations in lines propagated by single progeny descent). In this objective we will also test the hypothesis that sub-lethal insecticide exposure increases mutation rate by comparing how mutations accumulate in lines exposed to insecticide with insecticide unexposed lines. In the second objective we will use an approach called experimental evolution (the use of experimental populations exposed to specific conditions in the laboratory to study evolutionary processes) to examine the response of large clonal populations of M. persicae to insecticide selection. We will combine this approach with three different sequencing approaches to explore the molecular mechanisms underpinning evolved resistance, which will be validated in Objective 3 using functional approaches. The data from these experiments will fundamentally advance our understanding of how insects evolve in the absence of sex. Furthermore, the knowledge generated will be of considerable applied importance in relation to the sustainable control of aphid pests. For example, it will allow us to anticipate resistance risk development in countries where aphids reproduce asexually and optimise pesticide dosing strategies to avoid accelerating the evolution of mutations that might lead to resistance. Finally, understanding how clonal pest populations evolve resistance at the molecular level may provide opportunities to exploit and counter this process by developing strategies against the underpinning mechanisms involved.