Resistance to diamide insecticides in lepidopteran pests

Abstract

Diamide insecticides were first commercialised in 2006 by the launch of the benzenedicarboxamide derivative flubendiamide, followed by the anthranilic diamides chlorantraniliprole and cyantraniliprole. They are particularly active against a number of destructive lepidopteran pests and selectively activate insect ryanodine receptors (RyR), which are large tetrameric ryanodine-sensitive calcium release channels located in the sarco- and endoplasmic reticulum in neuromuscular tissues. Within a few years on the market, this class of insecticide chemistry gained blockbuster status by accounting for more than $1.2 billion of the 2013 global insecticide sales. On the downside, selection pressure on high-risk pests increased due to the frequent use of diamides, and high levels of field resistance to these insecticides have recently been reported in lepidopteran pests, such as diamondback moth, Plutella xylostella, and tomato leaf miner, Tuta absoluta. Here we briefly summarise cases of diamide insecticide resistance by analysing the underlying mechanisms of resistance compromising diamide efficacy in both laboratory- and field-selected strains of a number of lepidopteran pests. By far one of the most intensely investigated species, with respect to the underlying molecular mechanisms of diamide insecticide resistance, is diamondback moth. One of the major mechanisms of resistance including its underlying genetics yet identified is based on target-site mutations located in the transmembrane domain of the insect RyR. Possible fitness costs and metabolic mechanisms of resistance based on elevated levels of detoxification enzymes are not well studied yet. Finally we briefly discuss the general implications of the mechanistic findings gathered in several studies for the implementation of diamide resistance management programmes.