Ecological Genetics of Insecticide and Acaricide Resistance

Roush, Richard T.; McKenzie, John A.

doi:10.1146/annurev.en.32.010187.002045

Cited by 837 publications

(538 citation statements)

References 37 publications

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“…However, we still do not have any information about the genetic origin of the five electrophoretically distinct forms of phenoloxidase identified in this study or their heritability. Abundant evidence from other systems suggests that rapid acquisition of high level resistance resulting from intense selection of the type seen in QXR oysters often results from changes to just one gene [29]. Hence, we are now undertaking a Mendelian genetic analysis to test whether PO b represents an allele of a single phenoloxidase gene that can be used as the target for further selective breeding.…”

Section: Discussionmentioning

confidence: 99%

Breeding for QX disease resistance negatively selects one form of the defensive enzyme, phenoloxidase, in Sydney rock oysters

Bezemer

Butt

Nell

et al. 2006

Fish & Shellfish Immunology

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Section: Discussionmentioning

confidence: 99%

Breeding for QX disease resistance negatively selects one form of the defensive enzyme, phenoloxidase, in Sydney rock oysters

Bezemer

Butt

Nell

et al. 2006

Fish & Shellfish Immunology

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“…However, here the cost of a causal resistance mutation can easily be missed in experimental designs that only look at a specific fitness component. Indeed, population growth depends on a multitude of interdependent life‐history traits (LHTs) and their cumulative effect on population dynamics can only be estimated via complex parameters such as fertility life table parameters (LTPs; Roush & McKenzie, 1987). The second approach, often referred to as a “population cage” experiment because of its analogy to the traditional cage studies investigating Drosophila melanogaster genetics, analyzes fitness differences by placing resistant and susceptible genotypes in direct competition (Moore, 1952).…”

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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“…Since insecticide resistance first occurred more than one century ago (Mullin and Scott, 1992), insect pest populations have shown resistance to almost all the insecticides applied, because of intense and world-wide insecticide application (Roush and McKenzie, 1987). Until now, biochemical and molecular genetic approaches have identified and characterized several resistance genes which contribute to the main mechanisms of insecticide resistance, including target-site insensitivity and increased degradation of insecticides (Morton, 1993;Oakeshott et al, 2003;ffrench-Constant et al, 2004;Hemingway et al, 2004).…”

Section: Introductionmentioning

confidence: 99%

Seasonal fluctuation in susceptibility to insecticides within natural populations of Drosophila melanogaster. II. Features of genetic variation in susceptibility to organophosphate insecticides within natural populations of D. melanogaster

2006

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To elucidate genetic variation in susceptibility to organophosphate insecticides within natural populations of Drosophila melanogaster , we conducted an analysis of variance for mortality data sets of isofemale lines (10-286 lines) used in the previous studies. Susceptibility of isofemale lines to the three organophosphate insecticides was continuously distributed within each natural population, ranging from susceptible to resistant. Analysis of variance showed highly significant variation among isofemale lines in susceptibility to each insecticide for each natural population. Significant genetic variances in susceptibility to the three chemicals were estimated for the Katsunuma population; 0.0529-0.2722 for malathion, 0.0492-0.1603 for prothiophos, and 0.0469-0.1696 for fenitrothion. Contrary to the consistent seasonal tendency towards an increase in mean susceptibility in the fall, reported in the previous study, genetic variances in susceptibility to the three organophosphates did not change significantly in 1997 but tended to increase by 2-to 5-times in 1998. We tested whether both the observed situations, maintenance and increase in genetic variance in organophosphate resistance, can be generated under circumstances in which the levels of resistance to the three organophosphates tended to decrease, by conducting a simulation analysis, based on the hypothesis that resistant genotypes have lower fitnesses than susceptible ones under the density-independent condition. The simulation analysis generally explained the pattern in the mean susceptibility and genetic variances in susceptibility to the three organophosphates, observed in the Katsunuma population of D. melanogaster . It was suggested that the differences in the frequencies of resistance genes in the summer population could affect the patterns in genetic variance in organophosphate resistance in the fall population.

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Ecological Genetics of Insecticide and Acaricide Resistance

Cited by 837 publications

References 37 publications

Breeding for QX disease resistance negatively selects one form of the defensive enzyme, phenoloxidase, in Sydney rock oysters

Breeding for QX disease resistance negatively selects one form of the defensive enzyme, phenoloxidase, in Sydney rock oysters

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

Seasonal fluctuation in susceptibility to insecticides within natural populations of Drosophila melanogaster. II. Features of genetic variation in susceptibility to organophosphate insecticides within natural populations of D. melanogaster

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