Cloning of a sodium channel gene and identification of mutations putatively associated with fenpropathrin resistance in Tetranychus urticae

Kwon, Deok Ho; Clark, J. Marshall; Lee, Si Hyeock

doi:10.1016/j.pestbp.2009.07.009

Cited by 64 publications

(74 citation statements)

References 26 publications

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“…3), but have not been previously described as components of PyR1 or PyR2. These 10 residues include three residues in PyR1 (F S from Blattella germanica (Pridgeon et al, 2002) and Plutella xylostella (Endersby et al, 2011);and L 2i26 V from Tetranychus urticae (Kwon et al, 2010). We mutated the 10 pyrethroid-sensing residues in PyR1 and PyR2, as well as some residues beyond PyR1 and PyR2 and explored the actions of DMT and PMT on the mutants.…”

Section: Resultsmentioning

confidence: 99%

Rotational Symmetry of Two Pyrethroid Receptor Sites in the Mosquito Sodium Channel

Nomura

Zhorov

et al. 2015

Mol Pharmacol

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Voltage-gated sodium channels are the primary target of pyrethroid insecticides. Although it is well known that specific mutations in insect sodium channels confer knockdown resistance (kdr) to pyrethroids, the atomic mechanisms of pyrethroid-sodium channel interactions are not clearly understood. Previously, computer modeling and mutational analysis predicted two pyrethroid receptors, pyrethroid receptor site 1 (PyR1) (initial) and pyrethroid receptor site 2 (PyR2), located in the domain interfaces II/III and I/II, respectively. The models differ in ligand orientation and the number of transmembrane helices involved. In this study, we elaborated a revised PyR1 model of the mosquito sodium channel. Computational docking in the K v 1.2-based open channel model yielded a complex in which a pyrethroid (deltamethrin) binds between the linker helix IIL45 and transmembrane helices IIS5, IIS6, and IIIS6 with its dibromoethenyl and diphenylether moieties oriented in the intra-and extracellular directions, respectively. The PyR2 and revised PyR1 models explained recently discovered kdr mutations and predicted new deltamethrin-channel contacts. Further model-driven mutagenesis identified seven new pyrethroid-sensing residues, three in the revised PyR1 and four in PyR2. Our data support the following conclusions: 1) each pyrethroid receptor is formed by a linker-helix L45 and three transmembrane helices (S5 and two S6s); 2) IIS6 contains four residues that contribute to PyR1 and another four to PyR2; 3) seven pairs of pyrethroid-sensing residues are located in symmetric positions within PyR1 and PyR2; and 4) pyrethroids bind to PyR1 and PyR2 in similar orientations, penetrating deeply into the respective domain interfaces. Our study elaborates the dual pyrethroid-receptor sites concept and provides a structural background for rational development of new insecticides.

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Section: Resultsmentioning

confidence: 99%

Rotational Symmetry of Two Pyrethroid Receptor Sites in the Mosquito Sodium Channel

Nomura

Zhorov

et al. 2015

Mol Pharmacol

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“…Specifically, we focused on P262T in the mitochondrial cytb associated with bifenazate resistance (Van Leeuwen et al., 2008), the combined effect of G314D and G326E in the GluCl channels associated with avermectin resistance (Dermauw et al., 2012; Kwon, Yoon, et al., 2010), L1024V in the VGSC associated with pyrethroid resistance (Kwon, Clark, et al., 2010), and I1017F in CHS1 associated with resistance to etoxazole, clofentezine, and hexythiazox (Demaeght et al., 2014; Van Leeuwen et al., 2012). Five LTPs [the net reproductive rate (R0), intrinsic rate of increase (rm), mean generation time ( T ), the finite rate of increase (LM) and the doubling time (DT)], and nine single‐generation LHTs (immature stage survivorship [ISS], developmental time, sex ratio, adult longevity, daily and total fecundity, length of pre‐, post‐, and oviposition periods) were analyzed and compared across a total of 15 lines.…”

Section: Introductionmentioning

confidence: 99%

Fitness costs of key point mutations that underlie acaricide target‐site resistance in the two‐spotted spider miteTetranychus urticae

Bajda

Riga

Wybouw

et al. 2018

Evolutionary Applications

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The frequency of insecticide/acaricide target‐site resistance is increasing in arthropod pest populations and is typically underpinned by single point mutations that affect the binding strength between the insecticide/acaricide and its target‐site. Theory predicts that although resistance mutations clearly have advantageous effects under the selection pressure of the insecticide/acaricide, they might convey negative pleiotropic effects on other aspects of fitness. If such fitness costs are in place, target‐site resistance is thus likely to disappear in the absence of insecticide/acaricide treatment, a process that would counteract the spread of resistance in agricultural crops. Hence, there is a great need to reliably quantify the various potential pleiotropic effects of target‐site resistance point mutations on arthropod fitness. Here, we used near‐isogenic lines of the spider mite pest Tetranychus urticae that carry well‐characterized acaricide target‐site resistance mutations to quantify potential fitness costs. Specifically, we analyzed P262T in the mitochondrial cytochrome b, the combined G314D and G326E substitutions in the glutamate‐gated chloride channels, L1024V in the voltage‐gated sodium channel, and I1017F in chitin synthase 1. Five fertility life table parameters and nine single‐generation life‐history traits were quantified and compared across a total of 15 mite lines. In addition, we monitored the temporal resistance level dynamics of populations with different starting frequency levels of the chitin synthase resistant allele to further support our findings. Three target‐site resistance mutations, I1017F and the co‐occurring G314D and G326E mutations, were shown to significantly and consistently alter certain fitness parameters in T. urticae. The other two mutations (P262T and L1024V) did not result in any consistent change in a fitness parameter analyzed in our study. Our findings are discussed in the context of the global spread of T. urticae pesticide resistance and integrated pest management.

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“…The first occurs through target site mutation, e.g. voltage‐gated sodium channels (VGSCs) for pyrethroid and fenpropathrin (Tsagkarakou et al ., 2009; Kwon et al ., 2010a), acetylcholinesterase (AChE) for organophosphates and carbamates (Khajehali et al ., 2010), the GABA receptor for abamectin (Kwon et al ., 2010b), and cytochrome b (cyt‐b) for bifenazate and acequinocyl (Van Leeuwen et al ., 2011). The second mechanism involves enhanced metabolism enzymes, such as carboxylesterases (CESs), glutathione‐S‐transferases (GSTs), or cytochrome P450 monooxygenases (P450s) (Stumpf & Nauen, 2001; Ran et al ., 2009; Niu et al ., 2011).…”

Section: Introductionmentioning

confidence: 99%

Transcriptome analysis of the citrus red mite, Panonychus citri, and its gene expression by exposure to insecticide/acaricide

Dou

et al. 2012

Insect Molecular Biology

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The citrus red mite, Panonychus citri, is known for its ability rapidly to evolve resistance to insecticides/acaricides and to adapt to hosts that produce toxins. In this study, we constructed an unprecedented four gigabase pair transcriptome of P. citri, which was assembled into 64 149 unique transcripts, the functions of which were annotated by five public databases. A total of 116 unique transcripts were identified as representatives of potential involvement in the detoxification of xenobiotics. Genes recorded to encoding insecticide/acaricide target proteins were also obtained from the P. citri transcriptome. In order to explore novel candidate genes potentially involved in the pesticide detoxification of P. citri, we also constructed digital gene expression libraries of short-term transcriptome responses of P. citri to pesticides, which resulted in the identification of 120 unique transcripts potentially associated with insecticide/acaricide detoxification. Our study will facilitate molecular research on pesticide resistance in citrus red mites, as well as in other phytophagous mites.

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Cloning of a sodium channel gene and identification of mutations putatively associated with fenpropathrin resistance in Tetranychus urticae

Cited by 64 publications

References 26 publications

Rotational Symmetry of Two Pyrethroid Receptor Sites in the Mosquito Sodium Channel

Rotational Symmetry of Two Pyrethroid Receptor Sites in the Mosquito Sodium Channel

Fitness costs of key point mutations that underlie acaricide target‐site resistance in the two‐spotted spider miteTetranychus urticae

Transcriptome analysis of the citrus red mite, Panonychus citri, and its gene expression by exposure to insecticide/acaricide

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