scholarly journals Association between Three Mutations, F1565C, V1023G and S996P, in the Voltage-Sensitive Sodium Channel Gene and Knockdown Resistance in Aedes aegypti from Yogyakarta, Indonesia

Insects ◽  
2015 ◽  
Vol 6 (3) ◽  
pp. 658-685 ◽  
Author(s):  
Juli Wuliandari ◽  
Siu Lee ◽  
Vanessa White ◽  
Warsito Tantowijoyo ◽  
Ary Hoffmann ◽  
...  
Keyword(s):  
Aedes Aegypti ◽  
Sodium Channel ◽  
Knockdown Resistance ◽  
Channel Gene ◽  
Sodium Channel Gene

scholarly journals Permethrin Resistance in Aedes aegypti Affects Aspects of Vectorial Capacity

Insects ◽  
2021 ◽  
Vol 12 (1) ◽  
pp. 71
Author(s):  
Tse-Yu Chen ◽  
Chelsea T. Smartt ◽  
Dongyoung Shin
Keyword(s):  
Aedes Aegypti ◽  
Sodium Channel ◽  
Mosquito Control ◽  
Vector Competence ◽  
Vectorial Capacity ◽  
Parental Population ◽  
Control Programs ◽  
Channel Gene ◽  
Sodium Channel Gene ◽  
Specific Pcr

Aedes aegypti, as one of the vectors transmitting several arboviruses, is the main target in mosquito control programs. Permethrin is used to control mosquitoes and Aedes aegypti get exposed due to its overuse and are now resistant. The increasing percentage of permethrin resistant Aedes aegypti has become an important issue around the world and the potential influence on vectorial capacity needs to be studied. Here we selected a permethrin resistant (p-s) Aedes aegypti population from a wild Florida population and confirmed the resistance ratio to its parental population. We used allele-specific PCR genotyping of the V1016I and F1534C sites in the sodium channel gene to map mutations responsible for the resistance. Two important factors, survival rate and vector competence, that impact vectorial capacity were checked. Results indicated the p-s population had 20 times more resistance to permethrin based on LD50 compared to the parental population. In the genotyping study, the p-s population had more homozygous mutations in both mutant sites of the sodium channel gene. The p-s adults survived longer and had a higher dissemination rate for dengue virus than the parental population. These results suggest that highly permethrin resistant Aedes aegypti populations might affect the vectorial capacity, moreover, resistance increased the survival time and vector competence, which should be of concern in areas where permethrin is applied.

A novel amino acid substitution in the para-sodium channel gene in Rhipicephalus microplus (Acari: Ixodidae) associated with knockdown resistance

2010 ◽  
Vol 52 (4) ◽  
pp. 377-382 ◽  
Author(s):  
Marcelino Aguirre ◽  
Adriana E. Flores ◽  
Genoveva Álvarez ◽  
Alberto Molina ◽  
Iram Rodriguez ◽  
...  
Keyword(s):  
Amino Acid ◽  
Sodium Channel ◽  
Amino Acid Substitution ◽  
Rhipicephalus Microplus ◽  
Knockdown Resistance ◽  
Channel Gene ◽  
Sodium Channel Gene

A novel F1552/C1552 point mutation in the Aedes aegypti voltage-gated sodium channel gene associated with permethrin resistance

2010 ◽  
Vol 96 (3) ◽  
pp. 127-131 ◽  
Author(s):  
Jintana Yanola ◽  
Pradya Somboon ◽  
Catherine Walton ◽  
Woottichai Nachaiwieng ◽  
La-aied Prapanthadara
Keyword(s):  
Aedes Aegypti ◽  
Sodium Channel ◽  
Point Mutation ◽  
Voltage Gated Sodium Channel ◽  
Voltage Gated ◽  
Channel Gene ◽  
Sodium Channel Gene

scholarly journals Physiological evidence that three known mutations in the para-sodium channel gene confer cypermethrin knockdown resistance in Rhipicephalus microplus

2020 ◽  
Author(s):  
Raquel Cossío-Bayúgar ◽  
Estefan Miranda-Miranda ◽  
Francisco Martínez Ibañez ◽  
Verónica Narváez Padilla ◽  
Enrique Reynaud
Keyword(s):  
Sodium Channel ◽  
Pyrethroid Resistance ◽  
Experimental System ◽  
Rhipicephalus Microplus ◽  
Susceptible Strain ◽  
Cattle Tick ◽  
Knockdown Resistance ◽  
Channel Gene ◽  
Sodium Channel Gene ◽  
Physiological Evidence

Abstract Background: Acaricide resistance is a central problem for the control of the cattle tick Rhipicephalus microplus . Genetic changes that confer resistance get fixed in the population, however, the physiological effects and phenotypes of these mutations are not always well understood or characterized. SNPs in the para-sodium channel gene that confer cypermethrin knockdown resistance ( kdr ) were identified in several arthropods, and homologous mutations have been reported in R. microplus populations. To our knowledge, R. microplus populations that have these homologous SNPs have been associated and correlated with pyrethroid resistance but there is no direct physiological evidence that their presence does confer kdr in this organism. Methods: Resistance profiles from resistant and susceptible strains used in this work were obtained using the larval packet discriminating dose assay. The relevant genomic regions of the para-sodium channel of these strains were amplified using standard PCR; SNPs were detected by sequencing the corresponding amplicons. Ovary response to cypermethrin exposure/treatment was evaluated using videometrical analysis. Results: In this work we present historical evidence that the pyrethroid resistance trait is stable in a resistant reference strain after many years without selection, thus suggesting that the primary resistance mechanism is caused by mutations fixed in the population. In our experimental system, the mechanism that allows the maintenance of the contraction of the ovary after treatment with pyrethroids, is likely to be mediated by a change in the structure of the presynaptic para-sodium channel. We found that the resistant strain has the G184C, the C190A and the T2134A mutations in the para-sodium channel gene. SNPs G184C and T2134A have been reported to be genetically linked in resistant populations and are always found together. These mutations were confirmed to be absent in the susceptible strain used as control. Finally, using videometric analysis, we demonstrate that cypermethrin blocks ovary contraction in cypermethrin-susceptible ticks. We also show that ovaries from populations that carry the kdr associated SNPs still contract at cypermethrin concentrations that completely block ovary contraction in the susceptible strain. The configuration of the experimental system excludes a xenobiotic detoxification mechanism. Conclusions: This is the first report that presents physiological evidence that the presence of the G184C, the C190A, and the T2134A mutations in the para-sodium channel correlates with the ability of maintaining muscle contractility in R. microplus when exposed to cypermethrin. These results confirm that these SNPs may confer cypermethrin resistance in this organism by avoiding presynaptic blockage that in turn causes flaccid muscle paralysis that is characteristic of this acaricide. This work also demonstrates that the videometric assay that we previously validated can be used to detect more rapidly than other assays that involve larval mortality kdr -like cypermethrin resistant tick strains, because adult preengorged females can be directly assayed after they are collected on the field without waiting until eggs are laid and the larvae eclose.

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