Selection at the diazinon resistance locus in overwintering populations of Lucilia cuprina (the Australian sheep blowfly)

McKenzie, John A.

doi:10.1038/hdy.1994.98

Cited by 48 publications

(41 citation statements)

References 28 publications

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“…Excluding a number of studies that have focused on mosquitoes [ Culex pipiens quinquefasciatus (Berticat, Boquien, Raymond, & Chevillon, 2002; Berticat et al., 2008; Gazave, Chevillon, Lenormand, Marquine, & Raymond, 2001), Aedes aegypti (Brito et al., 2013), and Anopheles gambiae (Diop et al., 2015)], the Australian blow fly L. cuprina (McKenzie, 1990, 1994), and the peach aphid Myzus persicae (Foster, Denholm, & Devonshire, 2000), the majority of previous work that assesses pesticide resistance‐related fitness costs in arthropods suffers from multiple design weaknesses [see also reviews by ffrench‐Constant and Bass (2017) and Kliot and Ghanim (2012)]. A common design flaw is the evaluation of genetically unrelated populations in the experimental setup.…”

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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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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show abstract

“…One sample (control) was held at 27 AE 1 8C, the other (experimental) at 8 AE 1 8C. These are the respective conditions for continuous and arrested development (McKenzie 1990(McKenzie , 1994. After four weeks the experimental sample was transferred to the control temperature.…”

Section: (B) Development Of Wandering Larvae To Adultsmentioning

confidence: 99%

“…cuprina overwinters as pre-pupae following temperature-dependent arrested development of wandering larvae. Signi¢cant mortality occurs during this stage of the life cycle (Foster et al 1975;Dallwitz & Wardaugh 1984) with dieldrin-resistant and unmodi¢ed diazinon-resistant phenotypes selected against at low temperature (McKenzie 1990(McKenzie , 1994. The relationship between low temperature stress and asymmetry was therefore investigated.…”

Section: Introductionmentioning

confidence: 99%

Stress and asymmetry during arrested development of the Australian sheep blowfly

McKenzie

1997

Proc. R. Soc. Lond. B

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The dieldrin and diazinon resistance systems of the Australian sheep blow£y (Lucilia cuprina) have been used previously to relate stress, departures from bilateral symmetry, developmental stability and relative ¢tness. These systems are now used to consider stress and asymmetry in a developmental context. Larval to adult development is shown to be signi¢cantly impaired after arrested development at 8 8C, however the asymmetry score of adults of a given genotype is similar after arrested or continuous development. Selection against dieldrin-resistant and unmodi¢ed diazinon-resistant genotypes occurs during arrested development because greater proportions of these genotypes pupate at 8 8C than do susceptible or modi¢ed diazinon-resistant genotypes. Pre-pupae of all genotypes complete development equally successfully when transferred from 8 8C to 27 8C. Adults fail to emerge when pupae formed at 8 8C undergo this temperature transition. Temperature-shift experiments show the asymmetry score is determined between pre-pupal and pupal stages of the life cycle. This stage occurs at 27 8C in arrested and continuously developing cultures providing an explanation for the independence of stress, selective mortality during developmental arrest and asymmetry score. The results emphasize the need for genetic, environmental and developmental data before an asymmetry phenotype can be directly related to developmental stability and relative ¢tness.

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“…Major mutations conferring resistance to insecticides may entail pleiotropic costs that lower the fitness of resistant phenotypes in the absence of insecticide treatments (Abedi & Brown, 1960;McKenzie et al, 1982;Carrière et al, 1994;Groeters et al, 1994;McKenzie, 1994). Such costs may arise from disruptive effects of the resistance mechanisms on pre-existing functions, or from overproduction of detoxification enzymes diverting energy normally allocated to the life history traits (Uyenoyama, 1986;Lenski, 1988;Roush & Daly, 1990;Carrière et a!., 1994).…”

Section: Introductionmentioning

confidence: 99%

Change in genetic architecture resulting from the evolution of insecticide resistance: a theoretical and empirical analysis

Carrière

Roff

1995

Heredity

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Under selection for insecticide resistance, the spread of a major resistance allele that has strong pleiotropic effects on life history characters will affect the genetic architecture of fitness. A model is developed showing that the spread of such an allele induces a change in the mean and in the additive genetic variance (heritability) of the life history characters, and in the genetic covariance (correlation) between these characters. The model was tested using a quantitative genetic study that compared, in a lepidopteran species (Choristoneura rosaceana), the genetic architecture of diapause propensity and larval weight within and among insecticidefree and insecticide-treated populations from the same geographical area. Significant genetic correlations between resistance to the insecticides and the life history traits were found within the populations, suggesting that the resistance allele(s) has pleiotropic effects on the life history characters. As resistance develops from an initial value of zero, the model predicts a positive relationship between the degree of resistance within the populations and, (1) the magnitude of the fitness costs, (2) the heritability of the life history traits, and (3) the absolute value of the genetic correlations between pairs of life history traits. All these predictions were confirmed. Moreover, the evolution of resistance apparently affected the environmental variance in larval weight. Hence, the novel evolution of insecticide resistance appears to result in major changes in the genetic architecture of fitness, which may limit to some extent the colonization of insecticide-treated habitats.

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Selection at the diazinon resistance locus in overwintering populations of Lucilia cuprina (the Australian sheep blowfly)

Cited by 48 publications

References 28 publications

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

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

Stress and asymmetry during arrested development of the Australian sheep blowfly

Change in genetic architecture resulting from the evolution of insecticide resistance: a theoretical and empirical analysis

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