CHRONIC, MULTI-GENERATIONAL EXPOSURE TO LOW DOSES OF IMIDACLOPRID: ITS EFFECTS ON CHEMICAL PRECONDITIONING AND MUTATION INDUCTION IN NICOTINIC ACETYLCHOLINE RECEPTORS IN MYZUS PERSICAE (HEMIPTERA: APHIDIDAE)

Abstract

Hormesis is a phenomenon whereby exposure to low or sublethal doses of a chemical, physical, or biological stressor stimulate or enhance biological processes in an organism. Hormesis is an evolutionarily conserved process thought to allow organisms to adapt to stress. Hormetic effects such as increased lifespan and increased reproduction induced by exposure to low dose chemical stressors have been well documented in many insect species. This is of interest in integrated pest management as insects are likely to be exposed to low dose chemical stresses from pesticides as they break down in the environment. Under the umbrella of hormesis is another phenomenon known as hormetic preconditioning, whereby exposure to low doses of stress prime organisms to better survive additional, more challenging levels of stress. This phenomenon could aid in the development of insecticide resistance. It has also been hypothesized that low levels of stress may hasten the development of pesticide resistance by increasing mutation frequencies in pests. My thesis examined low dose and hormetic priming and whether it manifests over time by exposing Myzus persicae to low doses of imidacloprid, over four generations. Individuals from each generation were then exposed to several, increasingly lethal concentrations of the insecticide, imidacloprid, or spirotetramat, which has a differing mode of action, to determine if and how low dose insecticide exposure primed the aphids to better survive additional, and variable chemical stresses. Insects exposed to low doses of imidacloprid were also subjected to dose response assays, which characterized the ability of exposed aphids to survive a wide range of subsequent insecticide concentrations. I also examined whether exposure to low doses of the insecticide, imidacloprid, over multiple generations, induced mutations in five subunits of the M. persicae nicotinic acetylcholine receptor, comprising the majority of the imidacloprid binding site. Exposure to mildly toxic concentrations of imidacloprid did not result in priming when insects were subsequently exposed to more toxic concentrations of imidacloprid and spirotetramat. Exposure to hormetic concentrations of imidacloprid did prime insects to better cope with subsequent imidacloprid stress after several generations, but not spirotetramat stress. Hormetic priming did not manifest in a transgenerational manner and only some individuals in the population subjected to hormetic concentrations of imidacloprid appeared to be adapting to the insecticide. Exposure to hormetic and mildly toxic concentrations of imidacloprid did not result in mutations in subunits of the nicotinic acetylcholine receptor. While hormesis poses a challenge to pest management, my findings suggest that the extent to which low dose exposures to chemical stress likely will not result in substantial pesticide adaptation over several generations.