Genetics and fitness costs of acaricide resistance in spider mites

Abstract

The identification of the complex molecular mechanisms that govern the development of acaricide resistance in mite pests allows for more efficient pest management strategies. In chapter 2 we present the first genome-wide sequence data set for the spider mite Panonychus ulmi, and investigate the molecular mechanism underlying spirodiclofen resistance. In chapter 3, we shed more light on the contribution of target-site mutations to resistance to Mitochondrial Electron Transport Inhibitors I (METI-Is) in the spider mite pest Tetranychus urticae. We gather a body of experimental evidence that supports a causal link between the H92R mutation and METI-I resistance. In chapter 4, we introduce a marker-assisted backcrossing approach to create T. urticae lines that share a common pesticide-susceptible genomic background, excluding 9 loci that carry mutations that are associated with resistance to avermectins, pyrethroids, mite growth inhibitors, and mitochondrial complex III inhibitors. By this approach, this study functionally validates previously reported target-site resistance mutations in T. urticae. Subsequently, in chapter 5, we further take advantage of these near-isogenic lines to investigate possible fitness costs that are associated with the well-characterized acaricide target- site resistance mutations. Findings reported in this thesis are important considering the global spread of acaricide resistance, and within an Integrated Pest Management context