Biochemical Genetics of Insecticide Resistance

Plapp, Frederick W.

doi:10.1146/annurev.en.21.010176.001143

Cited by 141 publications

(43 citation statements)

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“…Since, the resistance to deltamethrin in the selected strain was not suppressed completely by the use of PBO and DEF, there could be some other mechanisms responsible for the resistance to deltamethrin. For example, the knockdown resistance (kdr) and reduced penetration (pen) are two important mechanisms responsible in the pyrethroid resistance in different insect pests (Plapp 1976;Shono 1985;Dong and Scott 1991;Jamroz et al 1998;Liu and Yue 2001;Khan et al 2011). However, the role of these mechanisms in the development of deltamethrin resistance in the Delta-SEL strain needs to be further investigated.…”

Section: Discussionmentioning

confidence: 99%

Genetics and mechanism of resistance to deltamethrin in the house fly, Musca domestica L., from Pakistan

2015

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Deltamethrin (a pyrethroid insecticide) has widely been used against the house fly, Musca domestica, a pest found in livestock facilities worldwide. Although, cases of both metabolic and physiological resistance to deltamethrin have been reported in different parts of the world, no studies have been reported to characterize this resistance in house flies from Pakistan. In the present study, we investigated a field strain of house flies for potential to develop resistance to deltamethrin. Also, its stability, possible mechanisms and cross-resistance potential to other insecticides. Before the selection experiments, the field strain showed 8.41-, 3.65-, 8.39-, 2.68-, 19.17- and 5.96-fold resistance to deltamethrin, bifenthrin, lambda-cyhalothrin, chlorpyrifos, profenofos and spinosad, respectively, compared with the reference strain (Lab-susceptible). Continuous selection of the field strain (Delta-SEL) with deltamethrin for six generations (G1-G6) in the laboratory increased the resistance ratio to 176.34 after bioassay at G7. The Delta-SEL strain was reared for the next four generations without exposure to deltamethrin and bioassayed at G11 which revealed that the resistance was stable. The Delta-SEL strain at G7 showed cross-resistance to all other insecticides except spinosad, when compared to the bioassays before the selection experiment (G1). Crosses between Delta-SEL and Lab-susceptible strains revealed an autosomal and incomplete dominant mode of resistance to deltamethrin. A direct test using a monogenic inheritance model revealed that the resistance was governed by more than one factor. Moreover, synergism studies with the enzyme inhibitors PBO and DEF reduced the resistance to deltamethrin in the selected strain up to 2.51- and 2.19-fold, respectively, which revealed that the resistance was possibly due to microsomal oxidase and esterase activity. It is concluded that the resistance to deltamethrin was autosomal and incompletely dominant. The high cross-resistance of bifenthrin, lambda-cyhalothrin, chlorpyrifos and profenofos in the Delta-SEL strain suggests that other insecticides would be necessary to counter the resistance. These results are therefore suggestive for implications in the management of insecticide resistance in house flies.

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Section: Discussionmentioning

confidence: 99%

Genetics and mechanism of resistance to deltamethrin in the house fly, Musca domestica L., from Pakistan

2015

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“…Second, both arthropod and vertebrate nervous systems contain two pharmacologically distinguishable types of acetylcholine receptors--the muscarinic receptors, which activate G-proteins, and the nicotinic receptors, which form an ion channel (Eldefrawi 1976;Jones et al 1979;Bonner 1989), and insect nicotinic and muscarinic receptors show specific sequence similarity to their vertebrate homologues (Hermans-Borgmeyer et al 1986;Onai et al 1989;Shapiro et al 1989b). Third, released acetylcholine is metabolized by a specific acetylcholinesterase enzyme, which is inactivated by the same organophosphate and carbamate pesticides in both arthropods and vertebrates (Plapp 1976). These organophosphates and carbamates act as substrates for acetylcholinesterase, and in the process they inactivate this enzyme by a covalent reaction with a critical serine residue at the active site (O'Brien 1976;Fukuto 1979).…”

Section: The Divergence Of Muscarinic Acetylcholine Receptors From Camentioning

confidence: 99%

The evolutionary divergence of neurotransmitter receptors and second-messenger pathways

Fryxell

1995

J Mol Evol

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Members of the superfamily of G-protein-coupled neurotransmitter receptors have a conserved secondary structure, a moderate and reasonably steady rate of sequence change, and usually lack introns within the coding sequence. These properties are advantageous for evolutionary studies. The duplication and divergence of the genes in this gene family led to the formation of distinct neurotransmitter pathways and may have facilitated the evolution of complex nervous systems. I have analyzed this evolutionary divergence by quantitative multiple sequence alignment, bootstrap resampling, and statistical analysis of 49 adrenergic, muscarinic cholinergic, dopamine, and octopamine receptor sequences from 12 animal species. The results indicate that the first event to occur within this gene family was the divergence of the catecholamine receptors from the muscarinic acetylcholine receptors, which occurred prior to the divergence of the arthropod and vertebrate lineages. Subsequently, the ability to activate specific second-messenger pathways diverged independently in both the muscarinic and the catecholamine receptors. This appears to have occurred after the divergence of the arthropod and vertebrate lineages but before the divergence of the avian and mammalian lineages. However, the second-messenger pathways activated by adrenergic and dopamine receptors did not diverge independently. Rather, the ability of the catecholamine receptors to bind to specific ligands, such as epinephrine, norepinephrine, dopamine, or octopamine, was repeatedly modified in evolutionary history, and in some cases was modified after the divergence of the second-messenger pathways.

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“…However, it was not until .30 years later that this activity was shown to be associated with one of the GSTs (Clark and Shamaan 1984). Since that time both qualitative and quantitative changes in GST-associated enzyme activity have been associated with resistance to organophosphorus, organochlorine, and pyrethroid insecticides (Ahmad and Forgash 1976;Plapp 1976;Li et al 2007). More recently, it has also been been inferred that GSTs can actually play two different roles in insecticide metabolism, the first by actually binding and sequestering insecticides and the second by protecting against oxidative stress when this is a by-product of insecticidal toxicity, such as with the pyrethroids (Vontas et al 2001(Vontas et al , 2002.…”

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confidence: 99%

The Molecular Genetics of Insecticide Resistance

2013

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The past 60 years have seen a revolution in our understanding of the molecular genetics of insecticide resistance. While at first the field was split by arguments about the relative importance of mono-vs. polygenic resistance and field-vs. laboratory-based selection, the application of molecular cloning to insecticide targets and to the metabolic enzymes that degrade insecticides before they reach those targets has brought out an exponential growth in our understanding of the mutations involved. Molecular analysis has confirmed the relative importance of single major genes in target-site resistance and has also revealed some interesting surprises about the multi-gene families, such as cytochrome P450s, involved in metabolic resistance. Identification of the mutations involved in resistance has also led to parallel advances in our understanding of the enzymes and receptors involved, often with implications for the role of these receptors in humans. This Review seeks to provide an historical perspective on the impact of molecular biology on our understanding of resistance and to begin to look forward to the likely impact of rapid advances in both sequencing and genome-wide association analysis."Curiouser and curiouser!" cried Alice.Lewis Carroll L ewis Carroll sent Alice down a rabbit hole without the least idea of what was to happen next, but as Alice ventured deeper into Wonderland things became "Curiouser and curiouser!" So indeed have studies on the molecular basis of insecticide resistance. While starting with rather simplistic expectations about the role of single mutations in single genes, resistance has been shown to involve a panoply of multiple mutations in multiple genes, often with independent and complex origins. This review will attempt to place these current findings into context and to examine the extent to which the field has often been historically blindsided by dogma. My arguments will encompass key controversies debated in the field such as the relative importance of mono-vs. polygenic resistance and the implications of resistance-associated mutations for whole-organism fitness in the absence of pesticide. Importantly, we will also examine the role of dogma in shaping the way that resistance research has been pursued over the past 50 years. Key questions addressed are therefore: How many mutations per gene cause resistance? How many mechanisms are there per species (genome)? How many independent genetic origins (mutations) give rise to each mechanism? What new mechanisms are still undiscovered and how might they arise? Monogenic vs. Polygenic ResistanceCrow, DDT, and DrosophilaThe humble fruit fly Drosophila melanogaster has been a key tool in unlocking the molecular basis of insecticide resistance, and early studies by James Crow and others have helped to establish Drosophila as a genetic model for resistance studies. Studies of DDT resistance in Drosophila have also typified arguments surrounding mono-vs. polygenic inheritance of insecticide resistance. In his pioneering review of in...

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Biochemical Genetics of Insecticide Resistance

Cited by 141 publications

References 0 publications

Genetics and mechanism of resistance to deltamethrin in the house fly, Musca domestica L., from Pakistan

Genetics and mechanism of resistance to deltamethrin in the house fly, Musca domestica L., from Pakistan

The evolutionary divergence of neurotransmitter receptors and second-messenger pathways

The Molecular Genetics of Insecticide Resistance

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