The biology of insecticidal activity and resistance

Perry, Trent; Batterham, Philip; Daborn, Phillip J.

doi:10.1016/j.ibmb.2011.03.003

Cited by 171 publications

(149 citation statements)

References 151 publications

(154 reference statements)

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“…The potential roles of the CNS, which is the site of the primary target of permethrin and the Malpighian tubules, fat body and midgut, which have a role in xenobiotic detoxification (Perry et al, 2011;Yang et al, 2007) were investigated. The LD 50 s of the tissue-specific knockdown strains relative to controls are shown in Fig.s 4-…”

Section: Knockdown Of Tryptophan Metabolism Enzymes Affects Survival mentioning

confidence: 99%

Metabolomic profiling of permethrin-treated Drosophila melanogaster identifies a role for tryptophan catabolism in insecticide survival

Brinzer

Henderson

Marchiondo

et al. 2015

Insect Biochemistry and Molecular Biology

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Insecticides and associated synergists are rapidly losing efficacy in target insect pest populations making the discovery of alternatives a priority. To discover novel targets for permethrin synergists, metabolomics was performed on permethrin-treated Drosophila melanogaster. Changes were observed in several metabolic pathways including those for amino acids, glycogen, glycolysis, energy, nitrogen, NAD + , purine, pyrimidine, lipids and carnitine.Markers for acidosis, ammonia stress, oxidative stress and detoxification responses were also observed. Many of these changes had not been previously characterized after permethrin exposure. From the altered pathways, tryptophan catabolism was selected for further investigation. The knockdown of some tryptophan catabolism genes (vermilion, cinnabar and CG6950) in the whole fly and in specific tissues including fat body, midgut and Malpighian tubules using targeted RNAi resulted in altered survival phenotypes against acute topical permethrin exposure. The knockdown of vermilion, cinnabar and CG6950 in the whole fly also altered survival phenotypes against chronic oral permethrin, fenvalerate, DDT, chlorpyriphos and hydramethylnon exposure. Thus tryptophan catabolism has a previously uncharacterized role in defence against insecticides, and shows that metabolomics is a powerful tool for target identification in pesticide research.

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Section: Knockdown Of Tryptophan Metabolism Enzymes Affects Survival mentioning

confidence: 99%

Metabolomic profiling of permethrin-treated Drosophila melanogaster identifies a role for tryptophan catabolism in insecticide survival

Brinzer

Henderson

Marchiondo

et al. 2015

Insect Biochemistry and Molecular Biology

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“…Third, nicotine is an extensively used addictive compound in humans, and nicotine dependence leads to a considerable number of tobacco-related, preventable deaths (Mokdad et al 2004;Jha et al 2013). The elite model organism Drosophila has proven a valuable system to understand the molecular genetics of drug responses (Kaun et al 2012) and pesticide resistance (Perry et al 2011). Indeed, one of the best described cases of the genetic control of xenobiotic resistance is the role of Cyp6g1 in resistance to the pesticide dichlorodiphenyltrichloroethane (DDT) in D. melanogaster.…”

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confidence: 99%

“…As a consequence of this strong evolutionary pressure, there are a number of examples of insecticide resistance arising in natural populations (Crow 1957). Understanding the biology and molecular genetics underlying resistance to insecticides (Perry et al 2011;Ffrench-Constant 2013) is valuable in the design of pest management strategies. In addition, humans are frequently exposed to an array of potentially harmful compounds, notably pharmaceuticals.…”

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confidence: 99%

Fine-Mapping Nicotine Resistance Loci inDrosophilaUsing a Multiparent Advanced Generation Inter-Cross Population

et al. 2014

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Animals in nature are frequently challenged by toxic compounds, from those that occur naturally in plants as a defense against herbivory, to pesticides used to protect crops. On exposure to such xenobiotic substances, animals mount a transcriptional response, generating detoxification enzymes and transporters that metabolize and remove the toxin. Genetic variation in this response can lead to variation in the susceptibility of different genotypes to the toxic effects of a given xenobiotic. Here we use Drosophila melanogaster to dissect the genetic basis of larval resistance to nicotine, a common plant defense chemical and widely used addictive drug in humans. We identified quantitative trait loci (QTL) for the trait using the DSPR (Drosophila Synthetic Population Resource), a panel of multiparental advanced intercross lines. Mapped QTL collectively explain 68.4% of the broad-sense heritability for nicotine resistance. The two largest-effect loci-contributing 50.3 and 8.5% to the genetic variation-map to short regions encompassing members of classic detoxification gene families. The largest QTL resides over a cluster of ten UDP-glucuronosyltransferase (UGT) genes, while the next largest QTL harbors a pair of cytochrome P450 genes. Using RNAseq we measured gene expression in a pair of DSPR founders predicted to harbor different alleles at both QTL and showed that Ugt86Dd, Cyp28d1, and Cyp28d2 had significantly higher expression in the founder carrying the allele conferring greater resistance. These genes are very strong candidates to harbor causative, regulatory polymorphisms that explain a large fraction of the genetic variation in larval nicotine resistance in the DSPR.A routine part of life for all organisms is avoiding, and if necessary metabolizing, toxic substances encountered in the environment. A common challenge for animals are those toxins produced by potential prey and plant hosts as chemical defenses against predation and herbivory (Glendinning 2002(Glendinning , 2007. Understanding how organisms overcome these defenses can give us insight into the evolution of host specialization, which can often involve an organism overcoming the defenses of a particular host, avoiding competition by making use of a resource toxic to other species (for example, Hungate et al. 2013). Many animals, especially insects, are also commonly exposed to chemical pesticides used to protect crop plants. As a consequence of this strong evolutionary pressure, there are a number of examples of insecticide resistance arising in natural populations (Crow 1957). Understanding the biology and molecular genetics underlying resistance to insecticides (Perry et al. 2011;Ffrench-Constant 2013) is valuable in the design of pest management strategies. In addition, humans are frequently exposed to an array of potentially harmful compounds, notably pharmaceuticals. Given the desire to achieve maximal drug efficacy while minimizing dosage and avoiding adverse drug responses, elaborating the mechanisms of drug metabolism, and the genet...

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“…However, due to the impacts and the development of strains resistant to the products, it has become necessary to use in rotation insecticides with different modes of action, as well as techniques that can assist in integrated pest management (IPM) (Jacobson et al, 2009;Gunning and Moores, 2010;Perry et al, 2011;Shind et al, 2011;Yang et al, 2013).…”

Section: Author(s) Agree That This Article Remain Permanently Open Acmentioning

confidence: 99%

Toxicity and sublethal effects of insecticides on Helicoverpa armigera Hbner (Lepidoptera: Noctuidae)

Carneiro¹,

Silva²,

Silva³

et al. 2016

Afr. J. Agric. Res.

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Exposure of Helicoverpa armigera to sublethal concentrations of insecticides can cause physiological deficiencies manifested by reduced longevity, development, fertility and fecundity. Research on the sub-lethal effects, to identify the non-lethal negative impacts of insecticides on pests can provide practical information for integrated management. The objective of this study was to determine the lethal concentrations and sublethal effects of insecticides on larval development and reproduction of H. armigera. The insecticides were diluted in water and applied via immersion of soybean leaf discs directly in the solution for three second, subsequently provided to the larvae maintained under controlled conditions for a period of 48 h. For surviving larvae, artificial diet was provided with daily evaluation until pupation. The pupae obtained were weighed after 24 h and transferred to Petri dishes, covered with filter paper until the adult phase, to evaluate longevity and pupal viability. For the assessments related to oviposition, couples were separated in polyvinyl chloride (PVC) cages and fed with 10% honey solution; the counting of eggs was done every two days, until the end of the oviposition period. All of the insecticides tested presented lethal and sublethal effects on the parameters weight, mortality and pupal viability and reduced oviposition and can be used in pest management, representing an alternative in the product rotation for the control of the third instar of H. armigera.

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The biology of insecticidal activity and resistance

Cited by 171 publications

References 151 publications

Metabolomic profiling of permethrin-treated Drosophila melanogaster identifies a role for tryptophan catabolism in insecticide survival

Metabolomic profiling of permethrin-treated Drosophila melanogaster identifies a role for tryptophan catabolism in insecticide survival

Fine-Mapping Nicotine Resistance Loci inDrosophilaUsing a Multiparent Advanced Generation Inter-Cross Population

Toxicity and sublethal effects of insecticides on Helicoverpa armigera Hbner (Lepidoptera: Noctuidae)

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