Indoxacarb and metaflumizone represent a new class of sodium channel-targeting insecticides known as sodium channel blocker insecticides (SCBIs). SCBIs preferably bind to sodium channels in the slow-inactivated (non-conducting) state and block the channels.  Due to intensive use of indoxacarb in control of a major vegetable pest, diamondback moth (Plutella xylostella), in China over the past 10 years, two sodium channel mutations have been discovered in indoxacarb-resistant diamondback populations. The two mutations, F4i15Y and V4i18I, are located in the transmembrane segment 6 of domain IV (IVS6). In this study, we introduced F4i15Y and V4i18I into a cockroach sodium channel and conducted functional analysis of the mutants in Xenopus oocytes. Both mutations reduced the inhibition of sodium current by DCJW (an active metabolite of indoxacarb) and metaflumizone, and also abolished the SCBI-induced hyperpolarizing shift in the voltage dependence of slow inactivation. In fact, the voltage-dependence of slow-inactivation of the SCBI-bound mutant channels was shifted in the depolarizing direction for both mutants.  These results indicate that both mutant channels are resistant to DCJW and metaflumizone, and likely confer diamondback moth resistance to SCBIs in the field. Elucidation of the molecular basis of SCBI resistance in various arthropod pests could guide future identification of the SCBI receptor on insect sodium channels.

Molecular basis of resistance to sodium channel blocker insecticides

248th National Meeting (2014)

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