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Mutations in the voltage-gated sodium channel gene associated with deltamethrin resistance in commercially sourced Phytoseiulus persimilis

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Open 2020_Benavent-Albarracin_Mutations_Post-print.pdf (3.011Mb)
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URI
http://hdl.handle.net/20.500.11939/6390
DOI
10.1111/imb.12642
URL
https://onlinelibrary.wiley.com/doi/abs/10.1111/imb.12642
Metadatos
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Autor
Benavent-Albarracín, Luís; Alonso-Valiente, Miquel; Catalán, José; Urbaneja, Alberto; Davies, T.G. Emyr; Williamson, Martin S.; González-Cabrera, Joel
Fecha
2020
Cita bibliográfica
Benavent‐Albarracín, L., Alonso, M., Catalán, J., Urbaneja, A., Davies, T. G. E., Williamson, M. S., & González‐Cabrera, J. (2020). Mutations in the voltage‐gated sodium channel gene associated with deltamethrin resistance in commercially sourced Phytoseiulus persimilis. Insect Molecular Biology, 29(4), 373-380.
Resumen
The implementation of Integrated Pest Management in current agricultural practice is a convenient and very effective strategy to keep pest populations under control. The use of biological control agents, such as Phytoseiulus persimilis, is key for the success of such an approach. This predatory mite is widely used as it is very effective for controlling Tetranychus urticae, one of the most devastating crop pests. Here, we identify several mutations located in the voltage‐gated sodium channel (VGSC) of commercially sourced P. persimilis that correlate with a reduced susceptibility to the pyrethroid deltamethrin. We found that the mites sourced from two different biocontrol product companies have intrinsic genotypic differences that correlate with their phenotype when tested with different concentrations of deltamethrin. Mites from Syngenta Bioline, carrying the mutations M918L and A1536T, were able to survive deltamethrin concentrations of up to 10 ppm, while the mites from Koppert Biological Systems, with the combination M918L, L925V and S1539T, survived treatment with 40 ppm. All of the point mutations identified in the predatory mite samples are located in a particular region of the VGSC, previously proposed as the binding site for this family of pesticides and identified as a ‘hot spot’ for resistance.
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