Differential resistance of insect sodium channels with kdr mutations to deltamethrin, permethrin and DDT

Burton, Mark J.; Mellor, Ian R.; Duce, I.R.; Davies, T.G. Emyr; Field, L. M.; Williamson, Martin S.

doi:10.1016/j.ibmb.2011.05.004

Cited by 95 publications

(77 citation statements)

References 43 publications

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“…gambiae), a significant additive benefit of 1575Y was detectable. 1014F and 1014S, although not directly in the binding pocket, are thought to produce their resistance phenotype through altering the confirmation of the VGSC, preventing binding of insecticide (9,24). By contrast, N1575Y occurs within the linker between domains III and IV, the site of the inactivation particle, a sequence of three amino acids (MFM in mammals and IFM in insects), which closes the sodium channel pore following activation, stopping influx of sodium ions into the cell so permitting restoration of the membrane resting potential.…”

Section: Discussionmentioning

confidence: 99%

“…24 and 28). Such electrophysiological studies have not only demonstrated the impact of 1014F and 1014S on neuronal response in the presence of insecticide but, additionally, indicated that, in the absence of insecticide, knockdown resistance mutations may exhibit different response profiles in comparison with wild-type alleles (24), which may manifest as a slight fitness detriment. In resistant bacteria, the costs of antibiotic resistance in the absence of selection pressure are known to be ameliorated by compensatory mutations co-occurring in the antibiotic target site (29).…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Footprints of positive selection associated with a mutation ( N1575Y ) in the voltage-gated sodium channel of Anopheles gambiae

Jones

Liyanapathirana²,

Agossa³

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

203

245

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Insecticide resistance is an ideal model to study the emergence and spread of adaptative variants. In the African malaria mosquito, Anopheles gambiae, this is complemented by a strong public health rationale. In this insect, resistance to pyrethroid and DDT insecticides is strongly associated with the mutations L1014F and L1014S within the para voltage-gated sodium channel (VGSC). Across much of West Africa, 1014F frequency approaches fixation. Here, we document the emergence of a mutation, N1575Y, within the linker between domains III-IV of the VGSC. In data extending over 40 kbp of the VGSC 1575Y occurs on only a single long-range haplotype, also bearing 1014F. The 1014F-1575Y haplotype was found in both M and S molecular forms of An. gambiae in West/ Central African sample sites separated by up to 2,000 km. In Burkina Faso M form, 1575Y allele frequency rose significantly from 0.053 to 0.172 between 2008 and 2010. Extended haplotype homozygosity analysis of the wild-type 1575N allele showed rapid decay of linkage disequilibrium (LD), in sharp contrast to the extended LD exhibited by 1575Y. A haplotype with long-range LD and high/increasing frequency is a classical sign of strong positive selection acting on a recent mutant. 1575Y occurs ubiquitously on a 1014F haplotypic background, suggesting that the N1575Y mutation compensates for deleterious fitness effects of 1014F and/or confers additional resistance to insecticides. Haplotypic tests of association suggest the latter: The 1014F-1575Y haplotype confers a significant additive benefit above 1014F-1575N for survival to DDT (M form P = 0.03) and permethrin (S form P = 0.003).kdr | selective sweep | inactivation particle

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Footprints of positive selection associated with a mutation ( N1575Y ) in the voltage-gated sodium channel of Anopheles gambiae

Jones

Liyanapathirana²,

Agossa³

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

203

245

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“…In addition, we also examined two mutations, leucine (L) to phenylalanine (F) or serine (S) mutation at amino acid position 1021 (L1021F/S) in domain II segment 6 (IIS6) because they were found in pyrethroid-resistant Anopheles and Culex mosquitoes (12). The L1021F mutation corresponds to L1014F in the house fly sodium channel and L993F in the cockroach sodium channel, both of which have previously been shown to reduce the sensitivity of respective sodium channels to pyrethroids (12,14), whereas the L1021S mutation reduces the sensitivity of a Drosophila sodium channel to pyrethroids (32). Because S996P and D1794Y mutations are often found to coexist with V1023G in pyrethroid-resistant field populations of Ae.…”

Section: Five Mutations Confer the Aana V 1-1 Channel Resistance To Pmentioning

confidence: 99%

Molecular evidence for dual pyrethroid-receptor sites on a mosquito sodium channel

Nomura

Satar

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

257

398

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Pyrethroid insecticides are widely used as one of the most effective control measures in the global fight against agricultural arthropod pests and mosquito-borne diseases, including malaria and dengue. They exert toxic effects by altering the function of voltage-gated sodium channels, which are essential for proper electrical signaling in the nervous system. A major threat to the sustained use of pyrethroids for vector control is the emergence of mosquito resistance to pyrethroids worldwide. Here, we report the successful expression of a sodium channel, AaNa v 1-1, from Aedes aegypti in Xenopus oocytes, and the functional examination of nine sodium channel mutations that are associated with pyrethroid resistance in various Ae. aegypti and Anopheles gambiae populations around the world. Our analysis shows that five of the nine mutations reduce AaNa v 1-1 sensitivity to pyrethroids. Computer modeling and further mutational analysis revealed a surprising finding: Although two of the five confirmed mutations map to a previously proposed pyrethroid-receptor site in the house fly sodium channel, the other three mutations are mapped to a second receptor site. Discovery of this second putative receptor site provides a dual-receptor paradigm that could explain much of the molecular mechanisms of pyrethroid action and resistance as well as the high selectivity of pyrethroids on insect vs. mammalian sodium channels. Results from this study could impact future prediction and monitoring of pyrethroid resistance in mosquitoes and other arthropod pests and disease vectors.

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“…As discussed previously, this is at least in part because while there are hundreds of different pesticides in use, they have a relatively small set of related molecular targets (Casida, 2009). For example, insects can develop cross‐resistance to DDT and pyrethroids because both of those classes of chemicals commonly inhibit voltage‐gated sodium channels in the central nervous system (e.g., Burton et al., 2011). Shared features of the chemical tolerance phenotype of the multiple tolerant killifish populations are analogous.…”

Section: Ecological Considerationsmentioning

confidence: 99%

When evolution is the solution to pollution: Key principles, and lessons from rapid repeated adaptation of killifish (Fundulus heteroclitus) populations

Whitehead

Clark

Reid

et al. 2017

Evolutionary Applications

120

102

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For most species, evolutionary adaptation is not expected to be sufficiently rapid to buffer the effects of human‐mediated environmental changes, including environmental pollution. Here we review how key features of populations, the characteristics of environmental pollution, and the genetic architecture underlying adaptive traits, may interact to shape the likelihood of evolutionary rescue from pollution. Large populations of Atlantic killifish (Fundulus heteroclitus) persist in some of the most contaminated estuaries of the United States, and killifish studies have provided some of the first insights into the types of genomic changes that enable rapid evolutionary rescue from complexly degraded environments. We describe how selection by industrial pollutants and other stressors has acted on multiple populations of killifish and posit that extreme nucleotide diversity uniquely positions this species for successful evolutionary adaptation. Mechanistic studies have identified some of the genetic underpinnings of adaptation to a well‐studied class of toxic pollutants; however, multiple genetic regions under selection in wild populations seem to reflect more complex responses to diverse native stressors and/or compensatory responses to primary adaptation. The discovery of these pollution‐adapted killifish populations suggests that the evolutionary influence of anthropogenic stressors as selective agents occurs widely. Yet adaptation to chemical pollution in terrestrial and aquatic vertebrate wildlife may rarely be a successful “solution to pollution” because potentially adaptive phenotypes may be complex and incur fitness costs, and therefore be unlikely to evolve quickly enough, especially in species with small population sizes.

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Differential resistance of insect sodium channels with kdr mutations to deltamethrin, permethrin and DDT

Cited by 95 publications

References 43 publications

Footprints of positive selection associated with a mutation ( N1575Y ) in the voltage-gated sodium channel of Anopheles gambiae

Footprints of positive selection associated with a mutation ( N1575Y ) in the voltage-gated sodium channel of Anopheles gambiae

Molecular evidence for dual pyrethroid-receptor sites on a mosquito sodium channel

When evolution is the solution to pollution: Key principles, and lessons from rapid repeated adaptation of killifish (Fundulus heteroclitus) populations

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