Genetics of Insect Resistance to Chemicals

Crow, James F.

doi:10.1146/annurev.en.02.010157.001303

Cited by 319 publications

(205 citation statements)

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“…Mutations that underlie target‐site resistance can carry a fitness disadvantage in an insecticide/acaricide‐free environment (Crow, 1957; Fisher, 1999). In contrast to target‐site resistance mutations that have been present within pest populations as natural balanced polymorphisms prior to the exposure of the insecticide/acaricide, de novo formed resistant alleles are expected to generate a high fitness disadvantage in resistant arthropods, compared to their susceptible conspecifics (ffrench‐Constant, 2007; ffrench‐Constant & Bass, 2017; Fisher, 1999).…”

Section: Discussionmentioning

confidence: 99%

“…In contrast to target‐site resistance mutations that have been present within pest populations as natural balanced polymorphisms prior to the exposure of the insecticide/acaricide, de novo formed resistant alleles are expected to generate a high fitness disadvantage in resistant arthropods, compared to their susceptible conspecifics (ffrench‐Constant, 2007; ffrench‐Constant & Bass, 2017; Fisher, 1999). In light of this theory, the study of the potential biological weaknesses that are associated with acaricide/insecticide resistance in populations is of high importance in the context of Insecticide Resistance Management (IRM; Crow, 1957; Georghiou & Taylor, 1977). The origin and history of the nucleotide polymorphisms associated with resistance remains largely unknown (but see Gould et al., 1997; Hartley et al., 2006), which lowers the reliability of a priori predictions of potential fitness costs.…”

Section: Discussionmentioning

confidence: 99%

“…Within the latter mechanism, nonsynonymous point mutations in the sequence coding for the pesticide target‐site are most often reported (Feyereisen, Dermauw, & Van Leeuwen, 2015). Theory predicts that de novo point mutations in essential target genes can convey pleiotropic effects, meaning they could affect other phenotypic traits in addition to pesticide resistance (ffrench‐Constant & Bass, 2017; Crow, 1957; Fisher, 1999). Indeed, these point mutations may, for instance, impose a structural constraint and put the conserved protein function and therefore the arthropod’s fitness at a disadvantage.…”

Section: Introductionmentioning

confidence: 99%

“…Pesticide resistance could thus result in fitness costs in populations that live in a pesticide‐free environment. As a consequence, alleviating pesticide use could result in a lower frequency of target‐site resistance alleles and, in turn, a lower resistance level of the population (Crow, 1957; Georghiou & Taylor, 1977). Target‐site resistance alleles can however be maintained in pest populations through several mechanisms.…”

Section: Introductionmentioning

confidence: 99%

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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: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

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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“…However, extensive attempts to demonstrate changes in D. pseudoobscura karotype fitness parameters due to insecticides have failed (Anderson et al, 1968). Genetic analysis of insecticide resistant populations of D. melanogaster have also failed to provide evidence that inversion polymorphism was involved, although they were not specifically designed to do so (Bochnig, 1954;Crow, 1957;King, 1958;King and Somme, 1958;Kikkawa, 1958;Ogaki and Tsukamoto, 1953;Tsukamoto and Ogaki, 1953;Oshima, 1958).…”

mentioning

confidence: 99%

ALDEHYDE OXIDASE ALLOZYMES, INVERSIONS AND DDT RESISTANCE IN SOME LABORATORY POPULATIONS OFDROSOPHILA MELANOGASTER

Laurie-Ahlberg¹,

Merrell²

1979

Evolution

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MATERIALS AND METHODSThe populations.-Two sets of populations were used in this study; one set has been selected for resistance to DDT (2,2-bis(p-chlorophenyl)-I, 1, l-trichloroethane) and the other consists of the corresponding control populations. They are designated as follows:ORC and ORR were derived in 1952 from the well-known stock Oregon R, which has been kept in the laboratory since at least 1925 (Bridges and Brehme, 1944). The pairs 731C and 731R and 91C and 91R were established in 1952 from collections of several hundred wild flies made in a residential area of St. Paul, Minnesota, about 1 month apart. The J populations were established from another studies of these populations have shown that a very high level of resistance has been achieved (Merrell, 1960;Dapkus and Merrell, 1977). The purpose of this report is to present evidence that (a) frequency changes of aldehyde oxidase (Ao) allozymes and the Payne inversion (In(3R)P) with which they are associated have occured in response to selection for DDT resistance and (b) the maintenance of the In(3R)P polymorphism at intermediate frequencies in selected populations is due to heterokaryotype advantage in survival that is specifically dependent on DDT in the environment.

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Biochemical Mechanisms of Resistance to Insecticides

Hodgson

Motoyama

1984

Ciba Foundation Symposium 102 ‐ Origins and Development of Adaptation

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Genetics of Insect Resistance to Chemicals

Cited by 319 publications

References 2 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

ALDEHYDE OXIDASE ALLOZYMES, INVERSIONS AND DDT RESISTANCE IN SOME LABORATORY POPULATIONS OFDROSOPHILA MELANOGASTER

Biochemical Mechanisms of Resistance to Insecticides

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