Abstract
The cotton bollworm, Helicoverpa armigera (Hübner) is one of the most serious insect pest species to evolve resistance against many insecticides from different chemical classes. This species has evolved resistance to the pyrethroid insecticides across its native range and is becoming a truly global pest after establishing in South America and having been recently recorded in North America. A chimeric cytochrome P450 gene, CYP337B3, has been identified as a resistance mechanism for resistance to fenvalerate and cypermethrin. Here we show that this resistance mechanism is common around the world with at least eight different alleles. It is present in South America and has probably introgressed into its closely related native sibling species, Helicoverpa zea. The different alleles of CYP337B3 are likely to have arisen independently in different geographic locations from selection on existing diversity. The alleles found in Brazil are those most commonly found in Asia, suggesting a potential origin for the incursion of H. armigera into the Americas.
Highlights
In agriculture, insecticides are commonly used to control insect pest species
Recent work confirmed a major incursion of H. armigera into Brazil, as well as Argentina, Uruguay and Paraguay and it has been detected in Puerto Rico and Florida [5,6,7,8]
The identification of H. armigera was initially based on morphological assessments by collectors and subsequently confirmed with the mitochondrial markers, cytochrome oxidase I and cytochrome b [29]
Summary
Insecticides are commonly used to control insect pest species. pest management is hindered by the increasing level of insecticide resistance in various pest species worldwide. One of the most serious insect pest species to evolve resistance against many insecticides from different chemical classes is the Old World cotton bollworm, Helicoverpa armigera (Hubner). Pyrethroid resistance of H. armigera was first reported in Australian populations in 1983, six years after the introduction of these insecticides [9]. Pyrethroid resistance has been reported from various populations globally but, in most cases, the molecular resistance mechanism in H. armigera is yet to be determined. The two major pyrethroid resistance mechanisms common to other species are target site insensitivity, and metabolic resistance by cytochrome P450 monooxygenases (P450s) and carboxylesterases [10, 11]. Target site resistance against pyrethroids, known as knockdown resistance (kdr), is based on one or more point mutations in the insect sodium channel protein, which is the target of pyrethroid insecticides. One of them is the chimeric CYP337B3, recently identified in Australian H. armigera and thought to have arisen through an unequal crossing-over between the parental genes, CYP337B1 and CYP337B2 [18]
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