Modeling Effects of Ecological Factors on Evolution of Polygenic Pesticide Resistance

Authors

C. V. Haridas, University of Nebraska-Lincoln
Brigitte Tenhumberg, University of Nebraska-LincolnFollow

Document Type

Article

Date of this Version

11-2018

Citation

Journal of Theoretical Biology 456 (November 2018), pp. 224–232.

doi: 10.1016/j.jtbi.2018.07.034

Comments

Copyright © 2018 Elsevier, Ltd. Used by permission.

Abstract

Widespread use of pesticides has resulted in the evolution of resistance in many insect pests worldwide, limiting their use in pest control. Effective pest and resistance management practices require understanding of the genetics of resistance and the life history of the pest. Most models for pesticide resistance assume that resistance is monogenic, conferred by a single gene. However, resistance could evolve as a polygenic quantitative trait resulting from the action of several genes, especially when pesticide dose is low. Further, fitness of the pest could be density dependent and might depend upon abiotic factors such as temperature. It is not known how these factors affect the evolution of polygenic resistance or pest population dynamics when resistance evolves. We use the western corn rootworm, Diabrotica virgifera virgifera, as a case study and use data on density-dependent survival, heritability, and survival rates on the transgenic Cry3Bb1 toxin and corresponding LC₅₀ values to model polygenic resistance to Cry3Bb1. We found that LC₅₀ increased rapidly even at doses that produced a mortality of less than 99.9%. However, survival reached 100% only when mortality was as high as 99.9%. Fast response to high selection pressure produced cyclical larval densities while lower selection pressures produced equilibrium densities. Interestingly, we found that a relatively low density observed in a population may not be evidence for a low survival to the pesticide. As a consequence we found that larger refuges might not necessarily help in reducing pest densities, especially when pesticide mortality is low. This effect, arising from the tradeoff between response to selection and density dependence, calls for careful assessment of the evolution of resistance based on change in survival as well as on pest densities. When selection pressure is low, a lower initial density resulted in a larger response to selection. Finally, we showed that populations with shorter developmental times developed resistance faster initially irrespective of selection pressure. However, when selection pressure is low, survival eventually became higher in populations with longer developmental times. Since developmental time depends on degree days spatiotemporal variation in temperature could be an important factor in polygenic resistance evolution.