Equivalent intensity but differential dominance of sodium channel blocker insecticide resistance conferred by F1845Y and V1848I mutations of the voltage-gated sodium channel in Plutella xylostella.

Two point mutations (F1845Y and V1848I) in the voltage-gated sodium channel gene of Plutella xylostella are involved in the target-site resistance to sodium channel blocker insecticides (SCBIs). The contribution of the individual mutations to the SCBI resistance and the associated inheritance modes is as yet unclear. Through 2 rounds of single-pair crossing and marker-assisted selection, 2 P. xylostella strains (1845Y and 1848I) bearing homozygous F1845Y or V1848I mutant alleles were successfully established from a field-collected population, and the contribution of each mutation to SCBI resistance, as well as associated inheritance patterns, was determined. When compared with the susceptible SZPS strain, each of the mutations individually conferred equally high-level resistance to indoxacarb (378 and 313 fold) and metaflumizone (734 and 674 fold), respectively. However, dominance levels of resistance to SCBIs were significantly different between the 2 resistant strains. Resistance of the 1845Y strain to indoxacarb and metaflumizone was inherited as an autosomal and incompletely dominant trait (D values ranged from 0.43 to 0.76). In contrast, that of the 1848I strain followed an autosomal but incompletely recessive to semidominant mode (D values: -0.24 to 0.09). Our findings enriched the current understanding of inheritance and mechanisms of SCBI resistance in P. xylostella, and will help develop resistance management programs for P. xylostella and other economic pests.