The Contribution of Detoxification Pathways to Pyrethroid Resistance in Hyalella Azteca

Author

Courtney Y. Fung, Southern Illinois University CarbondaleFollow

Date of Award

8-1-2018

Degree Name

Master of Science

Department

Zoology

First Advisor

Lydy, Michael

Abstract

Chronic exposure to pyrethroid insecticides can result in sublethal impacts to non-target species in aquatic systems, driving population-level changes. Characterizing the underlying mechanisms of resistance is essential to better understanding the role and potential consequences of contaminant-driven microevolution. The current study found that multiple mechanisms enhance the overall phenotypic expression of resistance characteristics in Hyalella azteca. In VGSC mutated H. azteca, both adaptation and acclimation traits appear to play a role in the attenuation of the adverse effects to pyrethroid exposures. Pyrethroid resistance is primarily attributed to the heritable mutation at various loci of the voltage-gated sodium channel, resulting in reduced target-site sensitivity. However, some additional reduced pyrethroid sensitivity was also conferred through reversible physiological responses to environmental conditions, such as enhanced enzyme-mediated detoxification. Cytochrome p450 monooxygenases (CYP450) and general esterases (GE) were the biotransformation pathways that significantly contributed to the detoxification of permethrin in H. azteca. Over time, VGSC mutated H. azteca retained most of their pyrethroid resistance, though there was some increased sensitivity from parent to offspring when reared in the absence of pyrethroid exposure. The permethrin 96 h LC50 declined from 1809 ng/L in P0 individuals to 1123 ng/L in the F1 generation, though still remained well above the 20.4 ng/L of wild-type individuals. This reduction in tolerance was likely related to alterations in acclimation mechanisms conferring resistance traits, rather than changes to target-site sensitivity. Enzyme bioassays indicated decreased CYP450 and GE enzyme activity from P0 to F1, whereas the VGSC mutation was retained. The permethrin LC50 values in resistant H. azteca were still two orders-of-magnitude higher than non-resistant populations indicating that the largest proportion of resistance was maintained through the inherited VGSC mutation. Thus, some variation in phenotypic expression of resistance characteristics in H. azteca over time is likely associated with uninheritable genetic factors or non-constitutively expressed traits controlling enzyme pathways which overlie a strong heritable component of resistance. A better understanding of the mechanistic and genomic basis of variable acclimation will be necessary for better predicting the ecological and evolutionarily consequences of contaminant-driven change in H. azteca.