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Reid, W.R., Sun, H., Becnel, J.J., Clark, A.G., Scott, J.G. (2019). Overexpression of a glutathione S-transferase (Mdgst) and a galactosyltransferase-like gene (Mdgt1) is responsible for imidacloprid resistance in house flies.  Pest Manag. Sci. 75(1): 37--44.
FlyBase ID
FBrf0240885
Publication Type
Research paper
Abstract

Neonicotinoids are the largest class of insecticides and are used for control of house fly populations at animal production facilities throughout the world. There have been several reports of neonicotinoid resistance in house fly populations, but identification of the factors involved in resistance has proven challenging. The KS8S3 population of house flies is highly resistant to the neonicotinoid insecticide imidacloprid due to two factors: one on chromosome 3 and one on chromosome 4. A comparative transcriptomic approach was used, followed by validation using transgenic Drosophila melanogaster to investigate the genes responsible for resistance in the KS8S3 strain. Overexpression of a microsomal glutathione S-transferase (Mdgst) was identified as the factor likely responsible for resistance on chromosome 3. Resistance on chromosome 4 appears to be due to an unidentified trans-regulatory gene which causes overexpression of a galactosyltransferase-like gene (Mdgt1). No single nucleotide polymorphisms were found that could be associated with imidacloprid resistance. Identification of the underlying processes that cause imidacloprid resistance is an important first step towards the development of novel and sensitive resistance monitoring techniques. It will be valuable to investigate if overexpression of Mdgst and Mdgt1 are found in other imidacloprid resistant populations. © 2018 Society of Chemical Industry.

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    Language of Publication
    English
    Additional Languages of Abstract
    Parent Publication
    Publication Type
    Journal
    Abbreviation
    Pest Manag. Sci.
    Title
    Pest Management Science
    Publication Year
    2000-
    ISBN/ISSN
    1526-498X
    Data From Reference
    Alleles (5)
    Genes (5)
    Natural transposons (1)
    Experimental Tools (1)
    Transgenic Constructs (5)