Abstract
The Colorado potato beetle (Leptinotarsa decemlineata (Say)) is a significant pest of potato plants that has been controlled for more than two decades by neonicotinoid imidacloprid. L. decemlineata can develop resistance to this agent even though the molecular mechanisms underlying this resistance are not well characterized. MicroRNAs (miRNAs) are short ribonucleic acids that have been linked to response to various insecticides in several insect models. Unfortunately, the information is lacking regarding differentially expressed miRNAs following imidacloprid treatment in L. decemlineata. In this study, next-generation sequencing and quantitative real-time polymerase chain reaction (qRT-PCR) were used to identify modulated miRNAs in imidacloprid-treated versus untreated L. decemlineata. This approach identified 33 differentially expressed miRNAs between the two experimental conditions. Of interest, miR-282 and miR-989, miRNAs previously shown to be modulated by imidacloprid in other insects, and miR-100, a miRNA associated with regulation of cytochrome P450 expression, were significantly modulated in imidacloprid-treated beetles. Overall, this work presents the first report of a miRNA signature associated with imidacloprid exposure in L. decemlineata using a high-throughput approach. It also reveals interesting miRNA candidates that potentially underly imidacloprid response in this insect pest.
Highlights
The Colorado potato beetle (CPB) (Leptinotarsa decemlineata (Say)) is a significant insect pest harming potato crops worldwide [1]
Efforts have been deployed in recent years to understand the molecular players associated with imidacloprid resistance in CPBs
Multiple studies have notably highlighted the differential expression of cytochrome P450s in imidacloprid-treated CPBs [9,10], positioning these enzymes as targets that could sensitize CBPs to this agent
Summary
The Colorado potato beetle (CPB) (Leptinotarsa decemlineata (Say)) is a significant insect pest harming potato crops worldwide [1]. Pest control strategies targeting CPBs typically involve pesticides, even though resistance against a variety of such compounds, including spinosad, thiamethoxam, and deltamethrin, has been observed [5,6,7]. Early studies reported adult CPBs exhibiting as much as a 155-fold increase in imidacloprid resistance in select populations [8]. Efforts have been deployed in recent years to understand the molecular players associated with imidacloprid resistance in CPBs. Multiple studies have notably highlighted the differential expression of cytochrome P450s in imidacloprid-treated CPBs [9,10], positioning these enzymes as targets that could sensitize CBPs to this agent. The complete molecular picture associated with imidacloprid resistance in CPBs remains incompletely characterized
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