Cyclodiene Insecticide Resistance: From Molecular to Population Genetics

Annual Review of Entomology - Tập 45 Số 1 - Trang 449-466 - 2000
Richard H. ffrench‐Constant1,2, Nicola M. Anthony3,2, Kate Aronstein3,2, Thomas A. Rocheleau3,2, Geoff Stilwell3,2
1Department of Biology and Biochemistry, University of Bath, United Kingdom. [email protected]
2Department of Entomology, University of Wisconsin-Madison, Wisconsin, 53706,
3Department of Biology and Biochemistry, University of Bath, Bath, BA2 7AY, United Kingdom

Tóm tắt

▪ Abstract  This review follows progress in the analysis of cyclodiene insecticide resistance from the initial isolation of the mutant, through cloning of the resistance gene, to an examination of the distribution of resistance alleles in natural populations. Emphasis is given to the use of a resistant Drosophila mutant as an entry point to cloning the associated γ-aminobutyric acid (GABA) receptor subunit gene, Resistance to dieldrin. Resistance is associated with replacements of a single amino acid (alanine302) in the chloride ion channel pore of the protein. Replacements of alanine302 not only directly affect the drug binding site but also allosterically destabilize the drug preferred conformation of the receptor. Resistance is thus conferred by a unique dual mechanism associated with alanine302, which is the only residue replaced in a wide range of different resistant insects. The underlying mutations appear either to have arisen once, or multiply, depending on the population biology of the pest insect. Although resistance frequencies decline in the absence of selection, resistance alleles can persist at relatively high frequency and may cause problems for compounds to which cross-resistance is observed, such as the novel fipronils.

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Annual Review of Entomology

Tập 45 Số 1

449-466

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