A novel amino acid substitution in a voltage-gated sodium channel is associated with knockdown resistance to permethrin in Aedes aegypti

Chang, Cheng‐Nan; Shen, Wen-Kai; Wang, Tzu-Ting; Lin, Yousheng; Hsu, Err-Lieh; Dai, Shu‐Mei

doi:10.1016/j.ibmb.2009.01.001

Cited by 124 publications

(136 citation statements)

References 30 publications

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“…Although these results might imply that both mutations are likely to be associated with deltamethrin resistance, more detailed analyses at a molecular level are required to resolve this issue. Six mutations (923, 982, 1011, 1016, 1552, and 1763) of domain II-III associated with pyrethroid resistance have been reported (Prapanthadara et al, 2002;Brengues et al, 2003;Saavedra-Rodriguez et al, 2007;Rajatileka et al, 2008;Chang et al, 2009;Kawada et al, 2009;Yanola et al, 2010). In this study, we identified the novel coexistence of the two mutations S989P and V1016G.…”

Section: Discussionmentioning

confidence: 54%

“…A similar scenario has been hypothesized for the D1763Y mutation in permethrin-resistant Ae. aegypti (Chang et al, 2009). Although we found that mosquitoes bearing both the S989P and V1016G mutations have shown a strong decrease in susceptibility 280 R. SRISAWAT et al to deltamethrin with increasing exposure time, we could not obtain direct evidence to discuss how these mutations are associated with resistance.…”

Section: Discussionmentioning

confidence: 99%

“…In addition, the coexistence of V1016G and D1763Y substitutions in domains II and III provided highly increasing knockdown resistance to permethrin in Ae. aegypti (Chang et al, 2009). Recently, an F1552C substitution of domain III was discovered in DDT/permethrin-resistant Ae.…”

Section: Introductionmentioning

confidence: 99%

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Point mutations in domain II of the voltage-gated sodium channel gene in deltamethrin-resistant Aedes aegypti (Diptera: Culicidae)

Srisawat

Komalamisra

Eshita

et al. 2010

Appl. Entomol. Zool.

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The continuous usage of pyrethroids against insects has provoked the emergence of insecticide resistance that has become a major obstacle to disease vector control. The knockdown resistance (kdr) voltage-gated sodium channel gene is regarded as a key to understanding the mechanism of resistance to pyrethroids. The main purpose of this study is to identify point mutations in the sodium channel gene associated with deltamethrin resistance in Aedes aegypti. Two mutations in the IIS6 domain of the channel, S989P and V1016G, were identified as possible candidates responsible for the emergence of deltamethrin resistance in Ae. aegypti Khu Bua strain. As S989P and V1016G mutations are located within the IIS5-S6 loop and IIS6 near the ion filter and binding site, these mutations might enhance pyrethroid resistance. Allelic variation in the sodium channel gene is thought to be one of the principal molecular mechanisms regulating pyrethroid resistance in mosquitoes.

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Section: Discussionmentioning

confidence: 54%

Section: Discussionmentioning

confidence: 99%

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Point mutations in domain II of the voltage-gated sodium channel gene in deltamethrin-resistant Aedes aegypti (Diptera: Culicidae)

Srisawat

Komalamisra

Eshita

et al. 2010

Appl. Entomol. Zool.

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“…The first mutation in the sodium channel that conferred resistance was detected in Musca domestica. subsequently mutations in other insects have been identified including Culicidae resistant to pyrethroids (Martínez et al, 1998;Brengues et al, 2003;Anstead, 2005;Saavedra et al, 2007;Brooke, 2008;Chang et al 2009;Yanola et al, 2010).…”

Section: Voltage-gated Sodium Channelmentioning

confidence: 99%

Susceptibility Status of Aedes aegypti to Insecticides in Colombia

Serrano¹

2012

Insecticides - Pest Engineering

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“…aegypti . 11,12 Multiple substitutions in the target site of DDT and the pyrethroid insecticides, the voltage-gated sodium channel on the insects' neurones, have also been described, 9,13,14 often referred to as kdr mutations (describing the knockdown resistance phenotype). However, only one of these, a valine to isoleucine substitution at codon 1016, has been clearly linked to insecticide resistance.…”

Section: Introductionmentioning

confidence: 99%

Pyrethroid Resistance in Aedes aegypti from Grand Cayman

Harris¹,

Rajatileka²,

Ranson³

2010

The American Society of Tropical Medicine and Hygiene

233

236

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The Grand Cayman population of Aedes aegypti is highly resistant to DDT and pyrethroid insecticides. Glutathione transferase, cytochrome P450, and esterase levels were increased in the Grand Cayman population relative to a susceptible laboratory strain, but synergist studies did not implicate elevated insecticide detoxification as a major cause of resistance. The role of target site resistance was therefore investigated. Two substitutions in the voltage-gated sodium channel were identified, V1016I in domain II, segment 6 (IIS6) (allele frequency = 0.79) and F1534C in IIIS6 (allele frequency = 0.68). The role of the F1534C mutation in conferring resistance to insecticides has not been previously established and so a tetraplex polymerase chain reaction assay was designed and used to genotype mosquitoes that had been exposed to insecticides. The F1534C mutation was strongly correlated with resistance to DDT and permethrin.

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A novel amino acid substitution in a voltage-gated sodium channel is associated with knockdown resistance to permethrin in Aedes aegypti

Cited by 124 publications

References 30 publications

Point mutations in domain II of the voltage-gated sodium channel gene in deltamethrin-resistant Aedes aegypti (Diptera: Culicidae)

Point mutations in domain II of the voltage-gated sodium channel gene in deltamethrin-resistant Aedes aegypti (Diptera: Culicidae)

Susceptibility Status of Aedes aegypti to Insecticides in Colombia

Pyrethroid Resistance in Aedes aegypti from Grand Cayman

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