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Based on the mode of action, the IGRs are classified into three major categories: i juvenile hormone mimics; ii ecdysone agonists; and iii chitin synthesis inhibitors [ 8 ]. Concerning the bacterial toxins, Bacillus thuringiensis Bs var. When ingested by larvae, the Bt toxins are activated by insect proteases and bind to specific receptors in the larvae midgut epithelia.

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The final effect is an osmotic stress that leads to the disruption of midgut membranes and, consequently, to death [ 9 ] [1] -. Insecticide resistance is considered the major challenge for control programs involving the use of chemicals. Up to , populations of at least species of insects were diagnosed as resistant to insecticides. Insecticide resistance has a genetic basis. Randomly arisen mutations can prompt several alterations in aspects of behavior, metabolism, and physiology of the insects, which may gain adaptive advantages in an insecticide-treated environment.

Such alterations can be classified as: i behavioral changes; ii altered penetration increased production of cuticular components that reduces intake of insecticide ; iii target site modification; and iv metabolic resistance detoxification enzymes and ABC transporters [ 10 ]. Although evidenced, the two first aspects are less reported, whilst several studies have described and evaluated the target site and metabolic resistance mechanisms.


These two, alone or combined, potentially induce a wide range of resistance levels to virtually all available insecticides [ 11 ]. Most insecticides target a single protein in the insect organism. The interaction between these molecules disrupts a normal biological process, leading to the toxicant effects. However, some mutations that induce structural alterations in the target protein can change the insecticide levels of toxicity.

Moreover, most of these alterations are conserved among distinct insect orders. For instance, cyclodienes inhibit chloride ion transport by keeping the gama-aminobutyric acid GABA receptor in a close conformation [ 12 ]. Interestingly, this mutation was never found in Aedes mosquitoes, regardless of the intense use of OP against their populations.

It means that in other mosquitoes a serine substitution AGC requires only one nucleotide change.

By contrast, two concomitantly selected mutations would be necessary in Aedes mosquitoes, an unlikely situation referred to as codon constraint [ 14 ]. Similarly, several mutations associated with PY and DDT resistance are present in distinct insect orders: the kdr mutations, that impair the knockdown effect provoked by those insecticides. The most common kdr knockdown resistance mutation is a leucine-to-phenylalanine substitution in the codon [1] - , although serine, histidine, cysteine, and tryptophan replacements are also found reviews presented in Rinkevich et al.

Several PY-resistant populations of major arthropod pests and disease vectors were found harboring kdr mutations. In this sense, for diagnostic purposes, different well-established tools for kdr genotyping have been implemented, specific for an increasing number of insect species. This allows a rapid and accurate access of the genetic background for PY resistance in natural populations [ 16 ]. The recent commercially introduced SP insecticides, which target the nicotinic acetylcholine receptors nAChRs [ 17 ], have been used for crop protection, animal health, and against human disease vectors.

However, resistance to this class of insecticides was already detected in a variety of insect species. A target-site point mutation glycine-to-glutamate substitution GE , for example, was identified in the nAChR of a Western flower thrips Frankliniella occidentalis in association with SP resistance [ 18 ]. As exemplified above, mutations selected for resistance in the molecular targets of insecticides generally share homologous sites among different insects.

These molecules are components of the nervous system, which are highly conserved among animals. Therefore, it is expected that few mutations can be maintained without impairing the essential physiological role of that molecule [ 20 ]. Target-site-resistant alleles are increasing in frequency and rapidly spreading, as well-recorded for malaria and dengue vectors. Detoxifying enzymes are naturally present in living organisms with a protective function against potential damages caused by xenobiotics and endogenous metabolites.

In many cases, insecticide resistance occurs due to an increased activity of such enzymes, a mechanism known as metabolic resistance. In general, this mechanism is related with the intense use of insecticides. However, other toxic compounds, such as chemical pollutants and plant toxins can also select for metabolic resistance mechanisms in insect populations. In this sense, different xenobiotics present in the environment are probably related, at least in part, with a preadaptation for insecticide resistance in disease vector and agricultural pests [ 21 , 22 ].

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Basically, xenobiotics pass through a series of enzymatic steps that transform them in polar substances, soluble in water for an easier excretion [ 23 ]. The biotransformation is divided into three phases, with the participation of three main groups of enzymes. Phase I includes multiple function oxidases enzymes MFO or P that carry out chemical modifications of a broad variety of xenobiotics. In phase II, glutathione S-transferases GST usually conduct conjugation reactions in the products resulting from the previous phase.

Finally, during phase III, the metabolites produced in the two first phases are actively exported out of the cells via ATP-binding cassette ABC transporters [ 24 - 27 ].

insecticide resistance

The metabolic resistance mechanisms are characterized by a gain in the ability for detoxifying molecules of insecticides, preventing them from reaching their targets. This acquisition can be selected by either an increase in the enzymatic activity over the insecticide mutations that improve the detoxifying power or an augment in the amount of copies of a specific enzyme due to an increase in the transcription rate, for instance. Glutathione S-transferases, EST and MFO P enzymes are each comprised of tens of genes, composing supergene families, possibly resulting from duplication events along the evolutionary process, as well as independent gene duplications inside distinct species [ 28 , 29 ].

Differently from target site mutations that can arise in homologous sites among different insect groups, several detoxifying genes are unique for some species and may be selected for insecticide resistance in a particular way. The main questions that lie upon the molecular basis of insecticide resistance mechanisms are how many and which genes control the phenotype of resistance, how many mutations were selected within that gene s , and if they are just spreading from one origin or appearing multiple times [ 30 ]. The advent of high-throughput screening molecular tools expands the searches for selected resistance mechanisms and their overall effects, toward beyond the target site mechanisms.

Recent advances have revealed the complexity of metabolic systems enrolled in insecticide resistance at transcriptomic and genomic levels. Comparisons of the whole transcriptional profile between susceptible and resistant individuals generally indicate the participation of several genes in the physiological process of resistance [ 31 - 33 ]. In addition, genetic loci influencing the resistance can be physically mapped in the chromosomes through quantitative trait loci QTL approaches [ 34 - 36 ].

Likewise, a recent study identified several single nucleotide polymorphisms SNPs , as well as an important and previously neglected copy number variation CNV related to insecticide resistance in Aedes aegypti , by combining genomic target enrichment with next-generation sequencing technologies [ 37 ]. Insecticide resistance is an adaptive trait in which a set of genes are favorably selected to maintain the insect alive and able to reproduce under an environment exposed to pesticides.

After being introduced, insecticides gradually eliminate the susceptible specimens, usually found at higher frequencies within populations. By contrast, harbors of resistant alleles, supposedly rare in the population, increase their frequencies along the time of continuous pesticide application. If resistance mechanisms hold elevated fitness cost in absence of insecticide as discussed subsequently , the rareness of these alleles in nonexposed populations is then a direct assumption.

In this case, the selection of resistance genes is a post adaptive response. On the other hand, pre adaptive selection of resistant alleles might have happened before the insecticide pressure, presumably if those alleles had another physiological role.

Consequently, this type of resistance alleles would be less likely to carry a fitness cost [ 39 ]. The presence of insecticides in the environment is the basis for resistance selection. Operational factors, like formulation, dosage, frequency, and intensity of application, will determine the strength of that selection pressure. Likewise, environmental and intrinsic biological elements will determine the extension and velocity for the dispersion course of resistance alleles.

The amount of resistance alleles and their initial frequency, as well as their dominance, penetrance, expressiveness, and interaction within the whole genetic background are the genetic components. In parallel, biological and ecological pieces in this scenario include the offspring size, generation turnover, mono or polygamy behaviors, together with degrees of mobility, isolation, and migration, mono or polyphagia, use of refuges, etc.

Naturally, the knowledge of most of these aspects will optimize the design for more effective insect control strategies. Even considering all those parameters, insecticide application can play a strong selection pressure, able to change the profile of a population very quickly [ 42 ]. One parameter that probably has a large impact on the evolution of insecticide resistance is the side effects, usually negative, related to the resistance mechanisms. This is likely the main reason that explains the low frequency of resistance alleles in populations not exposed to chemicals.

Therefore, the most common assumption is that when the use of insecticides is interrupted, the frequency of nonresistant specimens would tend to increase toward the establishment of the previous susceptibility levels of the population. This is especially what managers of campaigns against vector of pathogens anxiously look for, once the arsenal of insecticide compounds to this end is very restricted [ 4 , 5 ].

The mode of insecticide application is crucial to the velocity of resistance evolution. Since the main goal of these control strategies is a prompt reduction of the targeted insect population, they often apply high dosages of insecticides, which combined with the indiscriminate use of the household or agriculture products, result in a strong selective pressure.

If, as seems quite probable, similar sweeps have occurred in clusters containing resistant mutant Ps and GSTs [ 28 ], then a major reduction may have occurred in the genetic variation in this species' chemical defence system in a very short interval of evolutionary time. It must be said that the blowfly and some other major pests have proven remarkably adept in evolving resistance to many insecticides. As noted above, there may also be additional detoxification systems beyond the three major gene families so far studied. Nevertheless, it is tempting to suggest that, on top of any direct fitness costs in the absence of insecticide that may occur for some resistance mutants [ 25 ], there may also be a substantial 'opportunity cost' in terms of lost variation with which the species can respond to changes in its chemical environment in the future.


In conclusion, the application of genomic technologies to previously intractable cases of insecticide resistance has greatly expanded our views on the range of options available to insects to evolve insecticide resistance. On the other hand, however, we can also now see that the speed with which multiple resistance mutations are sweeping through some insect species will be substantially reducing the variation in linked genes.

In so far as many detoxification genes occur in tightly linked clusters, these selective sweeps will impinge on the genetic variation available to these species to respond to future insecticide or other xenobiotic challenges. Biochem J. Insect Biochem Molec Biol. Claudianos C, Russell RJ, Oakeshott JG: The same amino acid substitution in orthologous esterases confers organophosphate resistance on the house fly and a blowfly.

Vaughan A, Rocheleau T, ffrench-Constant R: Site-directed muta-genesis of an acetylcholinesterase gene from the yellow fever mosquito Aedes aegypti confers insecticide insensitivity. Exp Parasitol. Molec Gen Genet. Annu Rev Entomol. Feyereisen R: Insect P enzymes. Hemingway J: The molecular basis of two contrasting metabolic mechanisms of insecticide resistance. Trends Ecol Evol.

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In Ecological and Evolutionary Genetics of Drosophila. Download references. Correspondence to John G Oakeshott.