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  • Title: Electrical penetration graph technique as a tool to monitor the early stages of aphid resistance to insecticides.
    Author: Garzo E, Moreno A, Hernando S, Mariño V, Torne M, Santamaria E, Díaz I, Fereres A.
    Journal: Pest Manag Sci; 2016 Apr; 72(4):707-18. PubMed ID: 25989043.
    Abstract:
    BACKGROUND: Sulfoxaflor, a new insecticide from the sulfoximine chemical family, and imidacloprid, a widely used neonicotinoid insecticide, were tested to assess the susceptibility and feeding behaviour of two populations of Myzus persicae: Mp61, which exhibited target-site R81T resistance to neonicotinoids, and Mp1989, a laboratory clone maintained since 1989 as a susceptible reference. RESULTS: The imidacloprid LC50 value for Mp61 was 16 times higher than for Mp1989, showing a moderate level of resistance. Sulfoxaflor LC50 values for Mp61 and Mp1989 were much closer. The probing behaviour, as assessed by electrical penetration graphs (EPGs), of both populations was clearly altered by sulfoxaflor, which reduced the ability of aphids to find and feed from the phloem. The feeding behaviour of the susceptible Mp1989 population was much more severely affected than the moderately resistant Mp61 population on imidacloprid-treated plants. PCR assays of both aphid populations followed by DNA sequencing identified differences between populations in the point mutation in the β-subunit of the nicotinic acetylcholine receptor linked to the resistant gene against the neonicotinoid insecticide. CONCLUSIONS: Sulfoxaflor provoked feeding cessation more rapidly than imidacloprid in both aphid populations. Sharp differences in feeding behaviour were detected between the susceptible and the moderately resistant neonicotinoid-resistant aphid populations. The EPG technique can be used as a useful tool to give new insights into the functional effects of new chemical compounds and for early detection of low to moderate levels of resistance of sap-feeding insects to insecticides. The potential of this technique was validated by molecular analysis of the R81T mutation target site.
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