Mutations in Dα1 or Dβ2 nicotinic acetylcholine receptor subunits can confer resistance to neonicotinoids in Drosophila melanogaster

Perry, Trent; Heckel, David G.; McKenzie, John A.; Batterham, Philip

doi:10.1016/j.ibmb.2007.12.007

Cited by 71 publications

(75 citation statements)

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“…This mutant is referred to as Da1 KO . Given that previously created Da1 alleles are resistant to neonicotinoids (Perry et al 2008), Da1 KO was screened on two different neonicotinoids (imidacloprid and nitenpyram) and was found to be highly resistant to both ( Figure S2 and Table 1). Calculated LC50 values and resistance ratios were consistent with those measured for Da1 mutants studied previously (Perry et al 2008).…”

Section: Resultsmentioning

confidence: 99%

“…Given that previously created Da1 alleles are resistant to neonicotinoids (Perry et al 2008), Da1 KO was screened on two different neonicotinoids (imidacloprid and nitenpyram) and was found to be highly resistant to both ( Figure S2 and Table 1). Calculated LC50 values and resistance ratios were consistent with those measured for Da1 mutants studied previously (Perry et al 2008). Da1 and orthologs in pest species are well-established targets for several different neonicotinoid insecticides (Liu et al 2005;Perry et al 2008Perry et al , 2012.…”

Section: Resultsmentioning

confidence: 99%

“…melanogaster has 10 nAChR subunits; however, only three of these have been associated with behavioral phenotypes, with specific roles described for Da7 in the escape response (Fayyazuddin et al 2006) and for both Da3 and Da4 in sleep behavior (Shi et al 2014;Wu et al 2014). Mutations in three D. melanogaster nAChR subunits confer resistance to two important classes of insecticides; Da1 and Db2 to neonicotinoids (Perry et al 2008), and Da6 to spinosyns (Perry et al 2007Watson et al 2010;Somers et al 2015). Modification of an insecticide target protein can decrease the efficacy of an insecticide through altered affinity or pharmacological response (Ffrench-Constant et al 1993;Williamson et al 1996;Liu et al 2005).…”

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confidence: 99%

“…This could be particularly true for alleles that directly modify the neonicotinoid-binding site as neonicotinoids occupy the same binding site as ACh (Liu and Han 2006;Liu et al 2008). Loss-of-function mutants for the Da1, Da6, and Db2 genes are insecticide-resistant and viable (Perry et al 2007(Perry et al , 2008. The viability phenotype suggests a level of functional redundancy among nAChR subunits.…”

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confidence: 99%

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Pleiotropic Effects of Loss of the Dα1 Subunit in Drosophila melanogaster: Implications for Insecticide Resistance

et al. 2017

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Nicotinic acetylcholine receptors (nAChRs) are a highly conserved gene family that form pentameric receptors involved in fast excitatory synaptic neurotransmission. The specific roles individual nAChR subunits perform in Drosophila melanogaster and other insects are relatively uncharacterized. Of the 10 D. melanogaster nAChR subunits, only three have described roles in behavioral pathways; Da3 and Da4 in sleep, and Da7 in the escape response. Other subunits have been associated with resistance to several classes of insecticides. In particular, our previous work has demonstrated that an allele of the Da1 subunit is associated with resistance to neonicotinoid insecticides. We used ends-out gene targeting to create a knockout of the Da1 gene to facilitate phenotypic analysis in a controlled genetic background. To our knowledge, this is the first report of a native function for any nAChR subunits known to be targeted by insecticides. Loss of Da1 function was associated with changes in courtship, sleep, longevity, and insecticide resistance. While acetylcholine signaling had previously been linked with mating behavior and reproduction in D. melanogaster, no specific nAChR subunit had been directly implicated. The role of Da1 in a number of behavioral phenotypes highlights the importance of understanding the biological roles of nAChRs and points to the fitness cost that may be associated with neonicotinoid resistance.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

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confidence: 99%

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confidence: 99%

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Pleiotropic Effects of Loss of the Dα1 Subunit in Drosophila melanogaster: Implications for Insecticide Resistance

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“…22) Mutations or deletions of nAChRs can alter the toxicity of spinosad 12) or neonicotinoids. [23][24][25] However, no mutation of a nAChR has yet been reported to alter the toxicity to both spinosad and neonicotinoids.…”

Section: Spinosadmentioning

confidence: 99%

Unraveling the mystery of spinosad resistance in insects

Scott

2008

J. Pestic. Sci.

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SpinosadSpinosad (a mixture of spinosyns A and D, Fig. 1) is a new and highly promising insecticide, derived from the bacteria Saccharopolyspora spinosa, with efficacy against a wide range of insects. [1][2][3][4][5] The mechanism of action of spinosad appears to be unique, with a primary site of attack being the nicotinic acetylcholine receptor (nAChR) and a secondary site of attack being g-aminobutyric acid (GABA) receptors. [6][7][8][9][10][11] Spinosad is thought to exert its toxicity primarily by activating a nAChR (nAChN subtype). 9) Studies showing that deletion of the Da6 nAChR results in strains of Drosophila melanogaster that are highly resistant to spinosad 12) confirms the importance of nAChRs in spinosad toxicity. This unique mechanism(s) of action suggests that resistance due to changes in the target sites of other major insecticides (i.e. acetylcholinesterase and voltage sensitive sodium channel) would not result in cross-resistance to spinosad. This appears true for house flies and the oriental fruit fly (Bactrocera dorsalis) where only modest levels of cross-resistance to spinosad have been observed in laboratory strains and in field collected populations. [13][14][15][16][17] However, strains of Bactrocera dorsalis selected for resistance to organophosphates, carbamates or pyrethroids mechanisms unknown were up to 1000-fold cross-resistant to spinosad. 15) Nicotinic Acetylcholine ReceptorsNicotinic acetylcholine receptors (nAChR) belong to the Cysloop superfamily of ligand-gated ion channels that include gaminobutyric acid (GABA)-gated channels, glycine receptors, glutamate-gated Cl Ϫ channels and 5-hydroxytryptamine type Spinosad is a new and highly promising insecticide, derived from the bacteria Saccharopolyspora spinosa, with efficacy against a wide range of insects. The mechanism of action of spinosad appears to be unique, with a primary site of attack being the nicotinic acetylcholine receptor (nAChR) and a secondary site of attack being gaminobutyric acid (GABA) receptors. Neural nAChRs are composed of five subunits, with a minimum of 2 as. Each subunit possesses a large N-terminal extracellular domain that includes the acetylcholine (ACh) binding site and four transmembrane domains (M1-4) with M2 contributing most of the amino acids that line the ion channel. Spinosad resistance has been selected for and characterized in several insect species. Generally, resistance is monofactorial, recessive and cannot be overcome by insecticide synergists. Spinosad resistance in the house fly maps to chromosome 1 and three nAChR subunit genes (a5, a6, and b3) are predicted to exist on chromosome 1 based on Drosophila/Musca homology maps. However, cloning and sequencing of Mda5, Mda6, and Mdb3 from susceptible and spinosad resistant strains of house fly found no differences that could be associated with resistance. Unraveling the mystery of spinosad resistance in house flies will require further study. © Pesticide Science Society of Japan

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Cross‐resistance, inheritance and biochemical mechanisms of imidacloprid resistance in B‐biotype Bemisia tabaci

Wang

Yao

2009

Pest Management Science

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Although oxidative detoxification mediated by P450 monooxygenases is involved in imidacloprid resistance in the NJ-Imi strain of B-type B. tabaci, target-site modification as an additional resistance mechanism cannot be ruled out. Considering the high risk of cross-resistance, neonicotinoids should be regarded as a single group when implementing an insecticide rotation scheme in B. tabaci control.

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Mutations in Dα1 or Dβ2 nicotinic acetylcholine receptor subunits can confer resistance to neonicotinoids in Drosophila melanogaster

Cited by 71 publications

References 36 publications

Pleiotropic Effects of Loss of the Dα1 Subunit in Drosophila melanogaster: Implications for Insecticide Resistance

Pleiotropic Effects of Loss of the Dα1 Subunit in Drosophila melanogaster: Implications for Insecticide Resistance

Unraveling the mystery of spinosad resistance in insects

Cross‐resistance, inheritance and biochemical mechanisms of imidacloprid resistance in B‐biotype Bemisia tabaci

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