Inheritance mode and mechanisms of resistance to imidacloprid in the house fly Musca domestica (Diptera:Muscidae) from China

Abstract

Imidacloprid is a neonicotinoid insecticide that is effective against house fly, Musca domestica L., which is a major pest with the ability to develop resistance to insecticides. In the present study, we investigated the inheritance mode, the cross-resistance pattern and the mechanisms of resistance to imidacloprid. A near-isogenic house fly line (N-IRS) with 78-fold resistance to imidacloprid was used to demonstrate the mode of inheritance. The overlapping confidence limits of LC50 values and the slopes of the log concentration-probit lines between the reciprocal F1 and F1’ progenies suggest that imidacloprid resistance is inherited autosomally in the house fly. There was incomplete dominant inheritance in the F1 and F1’ progenies, based on dominance values of 0.77 and 0.75, respectively. A monogenic inheritance model revealed that imidacloprid resistance is governed by more than one factor. Compared to the field strain (CFD), the N-IRS strain developed more cross-resistance to chlorfenapyr and no cross-resistance to chlorpyrifos and acetamiprid, but showed negative cross-resistance to beta-cypermethrin and azamethiphos. Three synergists, diethyl malate (DEM), s,s,s-tributylphosphorotrithioate (DEF), and piperonyl butoxide (PBO), showed significant synergism against to imidacloprid (4.55-, 4.46- and 3.34-fold respectively) in the N-IRS strain. However, both DEM and PBO had no synergism and DEF only exhibited slight synergism in the CSS strain. The activities of carboxylesterase (CarE), glutathione S-transferases (GSTs) and cytochrome P450 in the N-IRS strain were significantly higher than in the CSS strain. But similar synergistic potential of DEF to imidacloprid between the CSS and N-IRS strain suggested that GSTs and cytochrome P450 played much more important role than esterase for the N-IRS strain resistance to imidacloprid. These results should be helpful for developing an improved management strategy to delay the development of imidacloprid resistance in house fly.

Inheritance and fitness costs of sulfoxaflor resistance in Nilaparvata lugens (Stål)

“…The number of genes involved in resistance is another important factor influencing the speed of evolution of resistance . According to our results, the significant difference between observed and expected mortalities of F 2 individuals suggested that sulfoxaflor resistance is governed by more than one allele.…”

“…Similarly, autosomal and incompletely recessive inheritance of resistance to imidacloprid has been observed for Musca domestica L. and Leptinotarsa decemlineata . Autosomal incompletely dominant imidacloprid resistance has also been reported in N. lugens , M. domestica and B‐type Bemisia tabaci . The different modes of inheritance may be because of variable insecticides, insect species, genetic background, environmental conditions, selection pressure history and the number of generations selected differed .…”

The role of G protein‐coupled receptor‐related genes in cytochrome P450‐mediated resistance of the house fly, Musca domestica (Diptera: Muscidae), to imidacloprid

“…Moreover, the transgenic line with the other eight upregulated genes in the N‐IRS or IRS strains did not lead to an increased level of resistance to imidacloprid, suggesting that it either is an indirect consequence of acquired imidacloprid resistance, or that the development of resistance requires the coordinated expression of many different genes so that overexpression of an individual gene is necessary, but perhaps not sufficient (Hu et al ., ). A previous study of ours showed that the N‐IRS strain possesses negative cross‐resistance to beta‐cypermethrin (Ma et al ., ); hence, increasing tolerance to beta‐cypermethrin was not found in the transgenic flies with LOC101899380 in the present study. Additionally, the D. melanogaster transgenic lines with LOC101899292 , LOC105262457 and LOC101891686 showed greater resistance to beta‐cypermethrin (3.07‐, 2.73‐ and 2.34‐fold, respectively), indicating that these genes may be related to beta‐cypermethrin resistance.…”

“…An imidacloprid‐resistant strain (IRS) was established from a field strain (CFD) by selection with imidacloprid for 21 generations in the laboratory, and showed a 155.8‐fold increased resistance compared to the CSS strain. The near‐isogenic line (N‐IRS) was obtained by crossing, backcrossing and self‐breeding between the CSS strain and the IRS strain, and developed 201‐fold resistance (Ma et al ., ). House flies were kept under standard laboratory conditions [25 ± 1 °C, 60–80% relative humidity (RH) and a 16 h:8 h light : dark photoperiod], and supplied with water, sugar, and milk powder.…”

“…Amongst the mechanisms responsible for imidacloprid resistance (IRS) in house flies, the overexpression of cytochrome (P450) genes (Markussen & Kristensen, 2010a; Højland et al ., ) and the underexpression of the nicotinic acetylcholine receptors (nAChR) subunit α2 (Markussen & Kristensen, 2010b) are known to play critical roles. Investigations into the synergism (piperonyl butoxide) and biochemical assays in house flies have shown that P450 plays a pivotal role in the IRS and N‐IRS strains' resistance to imidacloprid via increased expression of the P450 enzyme's activities (Ma et al ., ). P450 gene expression or induction in insecticide‐resistant insects is regulated by trans and/or cis factors (Li et al ., 2013b; Liu and Scott, ; King‐Jones et al ., ; Wan et al ., ; Ingham et al ., ) suggesting that insecticide resistance is conferred via the interaction of regulatory factors and resistance genes.…”