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Thesis Format



Master of Science




Grbic, Vojislava


In this investigation, etoxazole resistance was monitored in two spotted spider mite (TSSM) populations collected from commercial greenhouses in Ontario. The frequency of an etoxazole resistant, recessive target-site mutation, I1017F, in chitin synthase I (CHS1) was tracked within populations over the course of the study. Cytochrome P450 (P450) activity emerged as a possible alternative mechanism to resist etoxazole exposure in one population.

Using genetic crossing between highly resistant mite populations and a susceptible lab population, filial (F1) hybrid populations were created. The recessive I1017F target-site mutation was abolished in F1 hybrids highly susceptible to etoxazole, while elevated P450 activity was not retained throughout the investigation. My data reinforces the critical role the CHS1 I1017F mutation plays in etoxazole resistance in TSSM. Evidence for detoxification of etoxazole by P450s could not be separated from the dominant effect of the I1017F target-site mutation and further investigation into this possibility is required.

Summary for Lay Audience

Tetranychus urticae (Koch), the two spotted spider mite (TSSM), is a widespread agricultural pest with worldwide distribution. It is an extreme generalist, capable of feeding on at least 1100 plants species, including 150 economically important crops. TSSM is very small in size with adult females, the larger of the two sexes, being 0.5 mm long. With short generation time of 7-8 days in ideal conditions and adult females being able to lay (oviposit) up to 10-13 eggs a day, a small infestation of TSSM can quickly become a serious problem for commercial growers.

Commercial growers deploy biological controls (predatory mites) and acaricides (pesticides targeting acari species) to combat mite infestations. TSSM has been shown to rapidly evolve resistance to acaricides. This can result from a change in the sequence of the gene encoding a protein that is targeted by a pesticide, referred to as a target-site mutation. Metabolic resistance can also occur when detoxifying enzymes within the mite can break down or eliminate the acaricide before it can damage the mite.

The acaricide active ingredient of etoxazole is the focus of this investigation. A recessive target-site mutation, I1017F, within the chitin synthase I gene has been shown to be associated with etoxazole resistance. Metabolic resistance has been implicated in a few studies, but evidence is limited. This investigation monitored the resistance status of TSSM populations over time in relation to the I1017F mutation and looked for the presence of metabolic resistance.

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Creative Commons Attribution 4.0 License
This work is licensed under a Creative Commons Attribution 4.0 License.