Insecticide resistance resulting from an absence of target-site gene product

Thomas G. Wilson, Mudgapalli Ashok

Research output: Contribution to journalArticle

88 Citations (Scopus)

Abstract

Genetic changes in insects that lead to insecticide resistance include point mutations and upregulation/amplification of detoxification genes. Here, we report a third mechanism, resistance caused by an absence of gene product. Mutations of the Methoprene-tolerant (Met) gene of Drosophila melanogaster result in resistance to both methoprene, a juvenile hormone (JH) agonist insecticide, and JH. Previous results have demonstrated a mechanism of resistance involving an intracellular JH binding protein that has reduced ligand affinity in Met flies. We show that a γ-ray induced allele, Met27, completely lacks Met transcript during the insecticide-sensitive period in development. Although Met27 homozygotes have reduced oogenesis, they are viable, demonstrating that Met is not a vital gene. Most target-site resistance genes encode vital proteins and thus have few mutational changes that permit both resistance and viability. In contrast, resistance genes such as Met that encode nonvital insecticide target proteins can have a variety of mutational changes that result in an absence of functional gene product and thus should show higher rates of resistance evolution.

Original languageEnglish (US)
Pages (from-to)14040-14044
Number of pages5
JournalProceedings of the National Academy of Sciences of the United States of America
Volume95
Issue number24
DOIs
StatePublished - Nov 24 1998

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Methoprene
Insecticide Resistance
Juvenile Hormones
Insecticides
Genes
Oogenesis
Gene Amplification
Homozygote
Drosophila melanogaster
Point Mutation
Diptera
Insects
Carrier Proteins
Proteins
Up-Regulation
Alleles
Ligands
Mutation

ASJC Scopus subject areas

  • General

Cite this

Insecticide resistance resulting from an absence of target-site gene product. / Wilson, Thomas G.; Ashok, Mudgapalli.

In: Proceedings of the National Academy of Sciences of the United States of America, Vol. 95, No. 24, 24.11.1998, p. 14040-14044.

Research output: Contribution to journalArticle

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