Dr. William Reid’s presentation about pesticide resistance in the common house fly, Musca domestica, was another interesting talk in a colloquium series in which intrigue is entirely expected. But Dr. Reid’s presentation caught my attention particularly because of its focus on the mechanisms underlying an insect’s resistance to a commonly used synthetic pesticide that I’ve become increasingly more familiar with over the past couple of years: permethrin. I serve as a staff entomologist with a pest management company and as such I’m well aware that permethrin is not only widely used in structural pest management but also in agricultural and military applications and human and veterinary medicine.
Dr. Reid explained that though permethrin is widely used, and resistance to it has already mounted in several pest organisms, little is known of how the genes involved in metabolic resistance are regulated. Studies seem to suggest that insecticide resistance is mediated through a complex interplay of regulatory factors and is conferred via multiple gene up-regulation but no regulatory factors related to insecticide resistance had been identified until the research conducted by Dr. Reid and several other researchers at Auburn University. By working with a multiple pesticide resistant strain of house fly (ALHF) and two susceptible strains, aabys and CS, they were able to present compelling evidence that both interactions between autosomes and interactions within an autosome are important for the expression of genes that detoxify and subsequently confer resistance to permethrin.
The house fly has five autosomes (non-sex chromosomes), each of which contain genes involved in metabolic detoxification of pesticides and also genes that regulate the expression of pesticide resistance genes. Each of the five autosomes was individually substituted in the ALHF type (the highly insecticide resistant strain) with autosomes from CS or aabys (the pesticide susceptible strains). The individual contributions of each autosome were estimated by characterizing the changes in the gene expression levels of insecticide resistance genes as measured by the dose of the pesticide required to kill the fly. The substitution of certain autosomes could confer anything from two to over a thousand times resistance to permethrin or detract from an existing resistance to a significant degree. These findings suggest that insecticide resistance is mediated largely through interactions within an autosome and interactions between autosomes in addition to resistance conferred by the up-regulation of genes.
Dr. Reid’s research represents a much needed step forward in our understanding of the interplay of insect genetics and chemical suppression of insect populations. His work is part of an ongoing, concerted effort to understand the gene regulation and cellular signaling events that underpin insecticide resistance in insects; an effort that may lead to a better understanding of how insecticide cross-resistance develops and possibly novel ways to avoid it in the future.
Samuel Ramsey is a 2nd year PhD student in the Shrewsbury lab currently studying competition in egg parasitoids of the brown marmorated stink bug.