Insecticide resistance resulting from an absence of target-site gene product
AUTOR(ES)
Wilson, Thomas G.
FONTE
The National Academy of Sciences
RESUMO
Genetic changes in insects that lead to insecticide resistance include point mutations and up-regulation/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.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=24322Documentos Relacionados
- Tn10 insertion specificity is strongly dependent upon sequences immediately adjacent to the target-site consensus sequence.
- Rules for DNA target-site recognition by a lactococcal group II intron enable retargeting of the intron to specific DNA sequences
- Evolution of insecticide resistance in non-target black flies (Diptera: Simuliidae) from Argentina
- Site-specific cleavage of bacteriophage T4 DNA associated with the absence of gene 46 product function.
- The classification of esterases: an important gene family involved in insecticide resistance - A review