Article ID Journal Published Year Pages File Type
5514957 Pesticide Biochemistry and Physiology 2017 6 Pages PDF
Abstract

•Field strains developed low to moderate levels of resistance to imidacloprid and nitenpyram.•All strains were relatively susceptible to both dinotefuran and sulfoxaflor.•The full-length cDNA encoding Btβ1 was firstly cloned.•Deletion mutation was detected in JY strain.

Control of Bemisia tabaci has depended primarily and heavily on insecticides, especially neonicotinoids. The novel sulfoximine insecticide sulfoxaflor exhibits high potency against a broad range of sap-feeding insect species, including those resistant to neonicotinoids. The resistance levels of Q-biotype B. tabaci field strains collected from 8 locations in eastern China to neonicotinoids and sulfoxaflor were investigated, and single nucleotide polymorphisms (SNPs) of nicotinic acetylcholine receptor β1 subunit gene (Btβ1) were detected. Compared with the reference strain, the field strains had developed low to moderate levels of resistance to imidacloprid and nitenpyram with the resistance ratios (RR) ranging between 4.07 and 21.75-fold and 3.37 and 16.14-fold, respectively. While YZ strain exhibited high resistance (RF 40.38) to thiamethoxam, only low levels of resistance to thiamethoxam (RF 3.50-8.58) was observed in other strains. All strains were relatively susceptible to both dinotefuran (RF 0.50-2.55) and sulfoxaflor (RF 0.40-3.07). Sequence analysis of Btβ1 cDNA fragments revealed 23 SNPs representing 19 amino acid replacements in these strains. Notably, a 45 bp fragment deletion was detected in JY strain, which encodes 15 amino acid residues (positions 66-80) containing arginine at position 79 (R79) corresponding to the R81T mutation in Loop D of nAChR β1 subunit in Myzus persicae resistant to neonicotinoids. The lack of cross-resistance indicates that both dinotefuran and sulfoxaflor could play an important role in the control of B. tabaci already resistant to the first and second generation neonicotinoids.

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