Cis-Regulatory Elements in the Accord Retrotransposon Result in Tissue-Specific Expression of the Drosophila melanogaster Insecticide Resistance Gene Cyp6g1

Author:

Chung Henry12,Bogwitz Michael R12,McCart Caroline3,Andrianopoulos Alex2,ffrench-Constant Richard H4,Batterham Philip12,Daborn Phillip J12

Affiliation:

1. Centre for Environmental and Stress Adaptation Research, Bio21 Molecular Science and Biotechnology Institute

2. Department of Genetics, University of Melbourne, Melbourne, Victoria, 3010, Australia

3. Department of Biology and Biochemistry, University of Bath, Bath, BA2 7AY, United Kingdom and

4. Center for Ecology and Conservation, University of Exeter, Penryn, Cornwall, TR10 9EZ, United Kingdom

Abstract

Abstract Transposable elements are a major mutation source and powerful agents of adaptive change. Some transposable element insertions in genomes increase to a high frequency because of the selective advantage the mutant phenotype provides. Cyp6g1-mediated insecticide resistance in Drosophila melanogaster is due to the upregulation of the cytochrome P450 gene Cyp6g1, leading to the resistance to a variety of insecticide classes. The upregulation of Cyp6g1 is correlated with the presence of the long terminal repeat (LTR) of an Accord retrotransposon inserted 291bp upstream of the Cyp6g1 transcription start site. This resistant allele (DDT-R) is currently at a high frequency in D. melanogaster populations around the world. Here, we characterize the spatial expression of Cyp6g1 in insecticide-resistant and -susceptible strains. We show that the Accord LTR insertion is indeed the resistance-associated mutation and demonstrate that the Accord LTR carries regulatory sequences that increase the expression of Cyp6g1 in tissues important for detoxification, the midgut, Malpighian tubules, and the fat body. This study provides a significant example of how changes in tissue-specific gene expression caused by transposable-element insertions can contribute to adaptation.

Publisher

Oxford University Press (OUP)

Subject

Genetics

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