Point mutations in the insect voltage-sensitive sodium channel gene are postulated to confer knockdown resistance (kdr) to pyrethroids. One of these mutations, a methionine to valine replacement in the transmembrane segments IIS4-5 linker (analogous to the methionine to threonine substitution at position 918 of the house fly Vssc1 gene) was found in a resistant field population of Bemisia tabaci (Genn.) that was sampled in 1998. Using an allele-specific PCR assay, we evaluated the frequency of this mutation in two field and two laboratory populations of B. tabaci. For both field and laboratory populations, one population was resistant to the combination of fenpropathrin plus acephate while the other was susceptible. Although the frequency of the mutated allele was slightly higher in the resistant field population (12%) than in the susceptible field population (3%), the mutation was not found in the resistant or susceptible laboratory populations. Moreover, the mutated allele was detected in only one of 69 males surviving a discriminating concentration of fenpropathrin plus acephate. We therefore suggest that the methionine to valine replacement in the transmembrane segments IIS4-5 linker is not the target site modification underlying synergized pyrethroid resistance in Arizona B. tabaci. The possible involvement of other mutations in the voltage-sensitive sodium channel gene or the presence of a metabolic mechanism will be discussed.
Species 1: Homoptera Aleyrodidae Bemisia tabaci
Keywords: insecticide resistance, pyrethroids
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