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At least 19 recordsLinked to original sources
PubMed1997

Resistance to insecticides in insect vectors of disease: est alpha 3, a novel amplified esterase associated with amplified est beta 1 from insecticide resistant strains of the mosquito Culex quinquesfasciatus.

Vector control programmes in many countries face the dual problems of parasite drug resistance and insecticide resistance in the insect vectors of the disease. Here we report for the first time a new esterase-based insecticide resistance mechanism in the filariasis vector Culex quinquefasciatus. The field collected COL strain of C. quinquefasciatus from Columbia was heterogeneous for organophosphorus insecticide resistance. On native polyacrylamide gels it had an elevated beta-naphthyl acetate specific esterase with the same Rf as that for the Est beta 1s involved in insecticide resistance in other strains of this mosquito species. After five generations of temephos insecticide selection, both the esterase specific activity with p-nitrophenyl acetate and the temephos LC50 values were increased, suggesting that elevation of esterase activity was the underlying mechanism of resistance. Western blots with antisera raised to Est alpha 2(1) and Est beta 2(1) from C. quinquefasciatus indicated that the COL strain had an elevated Est alpha 3 enzyme which co-migrated on native gels with Est beta 1. Southern blots indicated that an est alpha 3 gene was amplified in the COL strain and a Cuban mosquito strain (MRes), although the restriction digest patterns of the est beta 1 genes in these two strains are different. In contrast, the Californian TEMR strain, with the amplified est beta 1(1) gene, had no associated elevated Est alpha. Restriction digest patterns for COL and TEMR DNA suggest that they contain an identical est beta 1(1) gene, but our data suggest that the est alpha 3 gene occurs on the same amplicon as an est beta 1 gene although the genes are probably > 10 kb apart. Hence, either the COL strain has two est beta 1 genes or the est beta 1(1) amplicon in TEMR has been disrupted at some stage during the long colonisation of this strain and the amplified est alpha has been lost.

Animals↗
PubMed2002

An overview of insecticide resistance.

Insecticide resistance poses a serious threat to current malaria control efforts. The Anopheles gambiae genome will enable identification of new resistance genes and will provide new molecular targets for the design of more effective insecticides.

Africa South of the Sahara↗
PubMed1959

Cross-resistance in insecticide-resistant strains of the German cockroach. Blattella germanica (L.

The authors describe a series of experiments designed to determine the extent to which cross-resistance exists in insecticide-resistant strains of the German cockroach. The tests were conducted by exposing females from a DDT-resistant strain, a chlordane-resistant strain, and a non-resistant strain to varying concentrations of several insecticides. From these tests mortality data were obtained and are presented in the form of regression lines.The insecticides used were DDT, methoxychlor, chlordane, dieldrin, Prolan, malathion, allethrin, and Lethane; these were chosen so that a wide variety of chemical types would be represented.The results indicate that the DDT-resistant strain is highly resistant to DDT and to its analogue, methoxychlor, but not to any of the other insecticides tested. Similarly, the chlordane-resistant strain is highly resistant to chlordane and to its analogue, dieldrin, but is susceptible to the other toxicants listed.From these results, as well as those obtained by others, it appears that the picture of cross-resistance in the German cockroach is in essential agreement with that which is emerging for other insects throughout the world.

Animals↗
PubMed1996

Polymerase chain reaction-based identification of insecticide resistance genes and DNA methylation in the aphid Myzus persicae (Sulzer).

The ability of a peach-potato aphid (Myzus persicae) to resist insecticides can depend on both the presence of amplified esterase genes and on differences in their expression. Here we report a polymerase chain reaction-restriction enzyme (PCR-REN) technique which can detect the presence of amplified esterase genes and distinguish between the two possible types of amplified gene (E4 and FE4) and a homologous fragment from susceptible aphids. The technique is quick and sensitive enough to be used on a fraction of an aphid or an individual embryo. Furthermore, it can be combined with a pre-PCR digestion using a methylation-sensitive enzyme (Hpall) to determine whether or not the esterase genes contain 5-methylcytosine, the presence or absence of which is known to correlate with changes in gene expression.

Animals↗
PubMed2004

Acetylcholinesterase alterations reveal the fitness cost of mutations conferring insecticide resistance.

BACKGROUND: Insecticide resistance is now common in insects due to the frequent use of chemicals to control them, which provides a useful tool to study the adaptation of eukaryotic genome to new environments. Although numerous potential mutations may provide high level of resistance, only few alleles are found in insect natural populations. Then, we hypothesized that only alleles linked to the highest fitness in the absence of insecticide are selected. RESULTS: To obtain information on the origin of the fitness of resistant alleles, we studied Drosophila melanogaster acetylcholinesterase, the target of organophosphate and carbamate insecticides. We produced in vitro 15 possible proteins resulting from the combination of the four most frequent mutations and we tested their catalytic activity and enzymatic stability. Mutations affected deacetylation of the enzyme, decreasing or increasing its catalytic efficiency and all mutations diminished the stability of the enzyme. Combination of mutations result to an additive alteration. CONCLUSION: Our findings suggest that the alteration of activity and stability of acetylcholinesterase are at the origin of the fitness cost associated with mutations providing resistance. Magnitude of the alterations was related to the allelic frequency in Drosophila populations suggesting that the fitness cost is the main driving force for the maintenance of resistant alleles in insecticide free conditions.

Acetylcholinesterase↗
PubMed1999

Cytochromes P450 and insecticide resistance.

The cytochrome P450-dependent monooxygenases (monooxygenases) are an extremely important metabolic system involved in the catabolism and anabolism of xenobiotics and endogenous compounds. Monooxygenase-mediated metabolism is a common mechanism by which insects become resistant to insecticides as evidenced by the numerous insect species and insecticides affected. This review begins by presenting background information about P450s, the role of monooxygenases in insects, and the different techniques that have been used to isolate individual insect P450s. Next, insecticide resistance is briefly described, and then historical information about monooxygenase-mediated insecticide resistance is reviewed. For any case of monooxygenase-mediated resistance, identification of the P450(s) involved, out of the dozens that are present in an insect, has proven very challenging. Therefore, the next section of the review focuses on the minimal criteria for establishing that a P450 is involved in resistance. This is followed by a comprehensive examination of the literature concerning the individual P450s that have been isolated from insecticide resistant strains. In each case, the history of the strain and the evidence for monooxygenase-mediated resistance are reviewed. The isolation and characterization of the P450(s) from the strain are then described, and the evidence of whether or not the isolated P450(s) is involved in resistance is summarized. The remainder of the review summarizes our current knowledge of the molecular basis of monooxygenase-mediated resistance and the implications for the future. The importance of these studies for development of effective insecticide resistance management strategies is discussed.

Animals↗
PubMed1997

Transposition-mediated transcriptional overexpression as a mechanism of insecticide resistance.

It has been proposed that amplification of genes for esterase that provide resistance to insecticides may originate from transposition events. To test this hypothesis, we have constructed a minigene coding for a soluble acetylcholinesterase under the control of a nontissue-specific promoter (hsp70). When introduced into Drosophila, the gene is expressed in all tissues and the extra acetylcholinesterase produced confers a low level of insecticide resistance (twofold). The minigene was mobilized by crossing the initial transformant with a strain providing a source of P-element transposase. After 34 generations of exposure to the organophosphate parathion, we obtained a strain with a higher resistance (fivefold). This strain had only one extra Ace gene, which overexpressed acetylcholinesterase. Thus, following transposition, resistance resulted from the overexpression of a single copy of the gene and not from gene amplification.

Acetylcholinesterase↗
PubMed1991

Gene mapping and cross-resistance in cyclodiene insecticide-resistant Drosophila melanogaster (Mg.).

Resistance to the cyclodiene insecticide dieldrin maps to a single gene (Rdl) on the left arm of chromosome III in Drosophila melanogaster (Meigen). The gene was further mapped by the use of chromosomal deficiencies to a single letter sub-region, 66F, on the polytene chromosome. The cross-resistance spectrum of a backcrossed strain lacking elevated mixed function oxidase activity, a common resistance mechanism, was examined. Levels of resistance similar to those found in other insects were found to dieldrin, aldrin, endrin, lindane, and picrotoxinin. Strong similarity of this single major gene with that found in other cyclodiene resistant insects is suggested by its cross-resistance spectrum and chromosomal location, via homology with other Diptera. The significance of major genes in insecticide resistance is discussed.

Animals↗
PubMed2004

The molecular basis of insecticide resistance in mosquitoes.

Insecticide resistance is an inherited characteristic involving changes in one or more insect gene. The molecular basis of these changes are only now being fully determined, aided by the availability of the Drosophila melanogaster and Anopheles gambiae genome sequences. This paper reviews what is currently known about insecticide resistance conferred by metabolic or target site changes in mosquitoes.

Animals↗
PubMed1998

Increased transcription of CYP6D1 causes cytochrome P450-mediated insecticide resistance in house fly.

Insecticide resistance is a major problem that continues to plague efforts to control pests of animals and crops. An important mechanism by which insects become resistant to insecticides is via increased detoxification mediated by the cytochrome P450 microsomal monooxygenases (monooxygenases). One of the fundamental gaps in our knowledge about this resistance mechanism is an understanding of how insects express high levels of the specific cytochrome P450(s) responsible for resistance. One such P450, CYP6D1, causes resistance to pyrethroid in the house fly and is expressed at 9-fold higher levels (mRNA and protein) in the Learn Pyrethroid Resistant (LPR) strain (compared to susceptible strains). The relative stability of CYP6D1 mRNA in resistant and susceptible strains was measured following inhibition of transcription with actinomycin D. The same time course of decrease in CYP6D1 mRNA abundance was detected in both strains indicating that the high level of expression of CYP6D1 in LPR is not due to increased stability of the mRNA. The comparative rates of transcription of CYP6D1 were measured using an in vitro run-on transcription assay. The relative amount of CYP6D1 transcript produced in this assay was 10-fold greater in the LPR strain compared to the susceptible strain. This demonstrates that increased transcription of CYP6D1 is an underlying cause of monooxygenase-mediated insecticide resistance. The increased rate of transcription of CYP6D1 in the resistant strain (LPR) is controlled by two factors: one on autosome 1 and another on autosome 2.

Animals↗
PubMed2002

A single p450 allele associated with insecticide resistance in Drosophila.

Insecticide resistance is one of the most widespread genetic changes caused by human activity, but we still understand little about the origins and spread of resistant alleles in global populations of insects. Here, via microarray analysis of all P450s in Drosophila melanogaster, we show that DDT-R, a gene conferring resistance to DDT, is associated with overtranscription of a single cytochrome P450 gene, Cyp6g1. Transgenic analysis of Cyp6g1 shows that overtranscription of this gene alone is both necessary and sufficient for resistance. Resistance and up-regulation in Drosophila populations are associated with a single Cyp6g1 allele that has spread globally. This allele is characterized by the insertion of an Accord transposable element into the 5' end of the Cyp6g1 gene.

Alleles↗
PubMed2002

Widespread insecticide resistance in head lice to the over-the-counter pediculocides in England, and the emergence of carbaryl resistance.

BACKGROUND: Increasing resistance to insecticides used for the control of head lice infestation has been documented over the last decade. Treatment failure and tolerance to insecticides have been validated in a number of studies undertaken in several U.K. centres. OBJECTIVES: To establish the extent of insecticide resistance in head lice and acetylcholinesterase activity in the presence of carbaryl in head lice. METHODS: Head lice were collected from school children in four centres across England (Exmouth, Loughborough, Leeds and South Shields), and tested in their response to the insecticides permethrin, phenothrin, malathion and carbaryl. Data were compared with information collected in Bristol and Bath in 1998 and with susceptible body lice. The activity of louse acetylcholinesterase was measured with and without carbaryl in head lice collected in Bristol, Leeds, Loughborough and in body lice. The efficacy of a 1% carbaryl lotion was compared in children in Bristol and Leeds. RESULTS: Compared with body lice, head lice from all six centres were significantly different in their response (P < 0.0001) to permethrin, phenothrin and malathion after 2-h exposure tests. There were significant differences in louse acetylcholinesterase activity in body lice, and head lice collected in Loughborough and Bristol in the presence or absence of carbaryl (P < 0.001), indicating enzyme inhibition. However, the difference for lice from Leeds was not significant (P = 0.363) suggesting that the enzyme was resistant to carbaryl. Eighty-nine per cent of children treated in Leeds with carbaryl were cured compared with 100% in Bristol. CONCLUSIONS: The data suggest head lice resistance is present in many parts of England to over-the-counter products containing synthetic insecticides (permethrin, phenothrin and malathion). They further suggest that resistance is starting to develop to carbaryl in head lice in Leeds and that extensive use of this product would lead to significant resistance.

Acetylcholinesterase↗
PubMed2003

Microarray analysis of cytochrome P450 mediated insecticide resistance in Drosophila.

Insecticide resistance in laboratory selected Drosophila strains has been associated with upregulation of a range of different cytochrome P450s, however in recent field isolates of D. melanogaster resistance to DDT and other compounds is conferred by one P450 gene, Cyp6g1. Using microarray analysis of all Drosophila P450 genes, here we show that different P450 genes such as Cyp12d1 and Cyp6a8 can also be selected using DDT in the laboratory. We also show, however, that a homolog of Cyp6g1 is over-expressed in a field resistant strain of D. simulans. In order to determine why Cyp6g1 is so widely selected in the field we examine the pattern of cross-resistance of both resistant strains and transgenic flies over-expressing Cyp6g1 alone. We show that all three DDT selected P450s can confer resistance to the neonicotinoid imidacloprid but that Cyp6a8 confers no cross-resistance to malathion. Transgenic flies over-expressing Cyp6g1 also show cross-resistance to other neonicotinoids such as acetamiprid and nitenpyram. We suggest that the broad level of cross-resistance shown by Cyp6g1 may have facilitated its selection as a resistance gene in natural Drosophila populations.

Animals↗
PubMed2000

Insecticide resistance and cross-resistance in the house fly (Diptera: Muscidae).

A house fly strain, ALHF, was collected from a poultry farm in Alabama after a control failure with permethrin, and further selected in the laboratory with permethrin for five generations. The level of resistance to permethrin in ALHF was increased rapidly from an initial 260-fold to 1,800-fold after selection. Incomplete suppression of permethrin resistance by piperonyl butoxide (PBO) and S,S,S,-tributylphosphorotrithioate (DEF) reveals that P450 monooxygenase- and hydrolase-mediated detoxication, and one or more additional mechanisms are involved in resistance to permethrin. The ALHF strain showed a great ability to develop resistance or cross-resistance to different insecticides within and outside the pyrethroid group including some relatively new insecticides. Resistance to beta-cypermethrin, cypermethrin, deltamethrin, and propoxur (2,400-4,200-, 10,000-, and > 290-fold, respectively, compared with a susceptible strain, aabys) in ALHF house flies was partially or mostly suppressed by PBO and DEF, indicating that P450 monooxygenases and hydrolases are involved in resistance to these insecticides. Partial reduction in resistance with PBO and DEF implies that multiresistance mechanisms are responsible for resistance. Fifteen- and more than fourfold resistance and cross-resistance to chlorpyrifos and imidacloprid, respectively, were not effected by PBO or DEF, indicating that P450 monooxygenases and hydrolases are not involved in resistance to these two insecticides. Forty-nine-fold cross-resistance to fipronil was mostly suppressed by PBO and DEF, revealing that monooxygenases are a major mechanism of cross-resistance to fipronil. Multiresistance mechanisms in the ALHF house fly strain, however, do not confer cross-resistance to spinosad, a novel insecticide derived from the bacterium Saccharopolyspora spinosa. Thus, we propose that spinosad be used as a potential insecticide against house fly pests, especially resistant flies.

Animals↗