Crowder, D.W., Department of Entomology, 410 Forbes Building, University of Arizona, Tucson, AZ, 85721, United States; Tabashnik, B.E., Department of Entomology, 410 Forbes Building, University of Arizona, Tucson, AZ, 85721, United States; Dennehy, T.J., Department of Entomology, 410 Forbes Building, University of Arizona, Tucson, AZ, 85721, United States; Denholm, I., Rothamsted Research, Harpenden, Hertfordshire AL5 2JQ, United Kingdom; Gorman, K., Rothamsted Research, Harpenden, Hertfordshire AL5 2JQ, United Kingdom; Carrire, Y., Department of Entomology, 410 Forbes Building, University of Arizona, Tucson, AZ, 85721, United States
We developed new methods for analyzing inheritance of insecticide resistance in haplodiploid arthropods and applied them to elucidate resistance of the whitefly Bemisia tabaci (Gennadius) to an insect growth regulator, pyriproxyfen. Two invasive biotypes of this devastating crop pest, the B biotype in Arizona and the Q biotype in Israel, have evolved resistance to pyriproxyfen. Here, we incorporated data from laboratory bioassays and crossing procedures exploiting haplodiploidy into statistical and analytical models to estimate the number of loci affecting pyriproxyfen resistance in strains of both biotypes. In tests with models of one to ten loci, the best fit between expected and observed mortality occurred with a two-locus model for the B biotype strain (QC-02) and for one- and two-locus models for the Q biotype strain (Pyri-R). The estimated minimum number of loci affecting resistance was 1.6 for the B biotype strain and 1.0 for the Q biotype strain. The methods used here can be applied to insecticide resistance and other traits in haplodiploid arthropods.
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