Professor University of Vermont Burlington, Vermont
Insect pests display an extraordinary ability to rapidly evolve resistance to insecticides. Although the evolution of insecticide resistance is widely considered to be inevitable, the underlying processes on how it occurs so rapidly remains poorly understood. One possible but largely unexplored explanation is that exposure to sublethal doses of insecticides may alter heritable epigenetic patterns. DNA methylation of cytosine nucleotides is one form of epigenetic modifications, which can alter heritable patterns of gene expression without changing the underlying genetic code. Therefore, sublethal exposure may influence the emergence of resistant phenotypes in complex ways. We assessed how exposure to sublethal doses of the neonicotinoid imidacloprid influences DNA methylation in the parent and F2 generations of Colorado potato beetle, Leptinotarsa decemlineata. We tested three imidacloprid treatments: a high dose, low dose, and an imidacloprid compound modified to be less toxic. We examined global changes in DNA methylation as well as individual differentially methylated sites. We found that all insecticide treatments decreased global DNA methylation in the parent and F2 generations, regardless of the dosage. Across all treatments exposed to insecticides, 221 nucleotide sites showed differential methylation. The majority, or 39% of these sites, were found in areas annotated as transposable elements. Given the consistent DNA methylation treatment patterns across the parent and F2 generation, our data demonstrates how environmental exposure to insecticides can have intergenerational carryover effects.
