Mechanisms Conferring Behavioral Resistance to the Neonicotinoid: Imidacloprid in the House Fly (Musca domestica Linnaeus)

The house fly (Musca domestica L.) is a cosmopolitan and synanthropic pest fly species commonly associated with confined animal facilities. It has been implicated in the transmission of over 200 different human and animal pathogens and can be extremely pestiferous in high numbers. One of the most common methods for house fly control is the use of insecticides, but insecticide resistance is an increasing problem due to over-application of insecticides and lack of rotation among insecticidal chemical classes. House fly resistance to imidacloprid, the most widely used neonicotinoid insecticide available for fly control, has evolved in field populations through both physiological and behavioral mechanisms. In this dissertation I investigated the mechanisms conferring behavioral resistance to imidacloprid. Behavioral resistance to imidacloprid was documented to present in a field population of flies from a southern California dairy, though the resistance was not uniform among individuals in the population. Flies were selectively bred for behavioral resistance to imidacloprid, without increasing the physiological resistance profile of the selected flies. The rapid selection for behavioral resistance suggests that inheritable alleles conferring behavioral resistance were already present in the wild type fly population collected from the dairy site. House fly behavioral resistance was further characterized using behavioral observation and feeding preference assays, with resistance determined to be both contact-dependent and specific to the insecticide (imidacloprid) rather than to a non-insecticidal component of a bait matrix as previously documented. The chromosomal location of behavioral resistance factors was then examined through the use of an autosomal linkage analysis. Behavioral resistance was mapped to autosomes 1 and 4 with inheritance of resistance being shown to be neither fully dominant nor recessive. Factors on autosomes 1 and 4 independently conferred contact-dependent avoidance and aversion of imidacloprid. The molecular mechanisms conferring behavioral resistance to imidacloprid were then investigated using a pooled sequencing approach. In this evolve and resequence experiment we attempted to identify putative selected sites or candidate loci that may be responsible for our selected phenotype by comparing house flies that did not exhibit the behavioral resistance phenotype to house flies that exhibited a high level of behavioral resistance. While 47 genes were identified to have significant differences in SNP frequencies between the susceptible and resistant populations, these genes either had an unknown function or a reported function that is not expected to alter expression of behavioral resistance to imidacloprid. Additional fundamental and applied research should be conducted to understand further both the complex phenotypic and genotypic nature of behavioral resistance to imidacloprid