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|Title:||Gene duplication in the major insecticide target site, Rdl, in Drosophila melanogaster|
|Citation:||Proceedings of the National Academy of Sciences of the United States of America, 2013; 110(36):14705-14710|
|Publisher:||National Academy of Sciences|
|Emily J. Remnanta, Robert T. Gooda, Joshua M. Schmidta, Christopher Lumba, Charles Robina, Phillip J. Daborna and Philip Batterhama|
|Abstract:||The Resistance to Dieldrin gene, Rdl, encodes a GABA-gated chloride channel subunit that is targeted by cyclodiene and phenylpyrazole insecticides. The gene was first characterized in Drosophila melanogaster by genetic mapping of resistance to the cyclodiene dieldrin. The 4,000-fold resistance observed was due to a single amino acid replacement, Ala(301) to Ser. The equivalent change was subsequently identified in Rdl orthologs of a large range of resistant insect species. Here, we report identification of a duplication at the Rdl locus in D. melanogaster. The 113-kb duplication contains one WT copy of Rdl and a second copy with two point mutations: an Ala(301) to Ser resistance mutation and Met(360) to Ile replacement. Individuals with this duplication exhibit intermediate dieldrin resistance compared with single copy Ser(301) homozygotes, reduced temperature sensitivity, and altered RNA editing associated with the resistant allele. Ectopic recombination between Roo transposable elements is involved in generating this genomic rearrangement. The duplication phenotypes were confirmed by construction of a transgenic, artificial duplication integrating the 55.7-kb Rdl locus with a Ser(301) change into an Ala(301) background. Gene duplications can contribute significantly to the evolution of insecticide resistance, most commonly by increasing the amount of gene product produced. Here however, duplication of the Rdl target site creates permanent heterozygosity, providing unique potential for adaptive mutations to accrue in one copy, without abolishing the endogenous role of an essential gene.|
|Rights:||For volumes 106–114 (2009–September 2017), the author(s) retains copyright to individual articles, and NAS retains an exclusive License to Publish these articles and holds copyright to the collective work. Volumes 90–105 (1993–2008) are copyright National Academy of Sciences. For volumes 1–89 (1915–1992), the author(s) retains copyright to individual articles, and NAS holds copyright to the collective work.|
|Appears in Collections:||Environment Institute publications|
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