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Pyrethroids, knockdown resistance and sodium channels
Author(s) -
Soderlund David M
Publication year - 2008
Publication title -
pest management science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.296
H-Index - 125
eISSN - 1526-4998
pISSN - 1526-498X
DOI - 10.1002/ps.1574
Subject(s) - housefly , knockdown resistance , pyrethroid , gene knockdown , biology , musca , genetics , pesticide resistance , toxicology , insecticide resistance , muscidae , gene , microbiology and biotechnology , pesticide , cyfluthrin , botany , ecology , larva
Knockdown resistance to DDT and the pyrethrins was first described in 1951 in the housefly ( Musca domestica L.). This trait, which confers reduced neuronal sensitivity to these insecticides, was subsequently shown to confer cross‐resistance to all synthetic pyrethroid insecticides that have been examined to date. As a consequence, the worldwide commercial development of pyrethroids as a major insecticide class over the past three decades has required constant awareness that pyrethroid overuse has the potential to reselect this powerful resistance mechanism in populations that previously were resistant to DDT. Demonstration of tight genetic linkage between knockdown resistance and the housefly gene encoding voltage‐sensitive sodium channels spurred efforts to identify gene mutations associated with knockdown resistance and understand how these mutations confer a reduction in the sensitivity of the pyrethroid target site. This paper summarizes progress in understanding pyrethroid resistance at the molecular level, with particular emphasis on studies in the housefly. Copyright © 2008 Society of Chemical Industry