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    Partitioning the roles of CYP6G1 and gut microbes in the metabolism of the insecticide imidacloprid in Drosophila melanogaster

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    Author
    Fusetto, R; Denecke, S; Perry, T; O'Hair, RAJ; Batterham, P
    Date
    2017-09-12
    Source Title
    Scientific Reports
    Publisher
    NATURE PUBLISHING GROUP
    University of Melbourne Author/s
    Batterham, Philip; Perry, Trent; O'Hair, Richard
    Affiliation
    School of Chemistry
    School of BioSciences
    Metadata
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    Document Type
    Journal Article
    Citations
    Fusetto, R., Denecke, S., Perry, T., O'Hair, R. A. J. & Batterham, P. (2017). Partitioning the roles of CYP6G1 and gut microbes in the metabolism of the insecticide imidacloprid in Drosophila melanogaster. SCIENTIFIC REPORTS, 7 (1), https://doi.org/10.1038/s41598-017-09800-2.
    Access Status
    Open Access
    URI
    http://hdl.handle.net/11343/256984
    DOI
    10.1038/s41598-017-09800-2
    Abstract
    Resistance to insecticides through enhanced metabolism is a worldwide problem. The Cyp6g1 gene of the vinegar fly, Drosophila melanogaster, is a paradigm for the study of metabolic resistance. Constitutive overexpression of this gene confers resistance to several classes of insecticides, including the neonicotinoid imidacloprid (IMI). The metabolism of IMI in this species has been previously shown to yield oxidative and nitro-reduced metabolites. While levels of the oxidative metabolites are correlated with CYP6G1 expression, nitro-reduced metabolites are not, raising the question of how these metabolites are produced. Some IMI metabolites are known to be toxic, making their fate within the insect a second question of interest. These questions have been addressed by coupling the genetic tools of gene overexpression and CRISPR gene knock-out with the mass spectrometric technique, the Twin-Ion Method (TIM). Analysing axenic larvae indicated that microbes living within D. melanogaster are largely responsible for the production of the nitro-reduced metabolites. Knock-out of Cyp6g1 revealed functional redundancy, with some metabolites produced by CYP6G1 still detected. IMI metabolism was shown to produce toxic products that are not further metabolized but readily excreted, even when produced in the Central Nervous System (CNS), highlighting the significance of transport and excretion in metabolic resistance.

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