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The mosquito larval midgut brush-border membrane receptors and epithelial cell membranes represent the critical site of action for biological insecticides used in the control of disease-carrying mosquitoes. This target complex consists of various proteins located on the apical microvilli of the larval midgut, including aminopeptidase N (APN), alkaline phosphatase (ALP), cadherin-like proteins, and ABC transporters such as ABCC2 [1, 2, 6]. These receptors are specifically recognized by the Cry and Cyt toxins produced by Bacillus thuringiensis israelensis (Bti) and Lysinibacillus sphaericus (Ls) [1, 3]. Following ingestion and proteolytic activation in the alkaline larval gut, these toxins bind to the receptors, which facilitates their oligomerization and insertion into the epithelial cell membrane [1, 4]. This insertion forms pores that disrupt osmotic regulation, leading to cell swelling, lysis, and the rapid death of the larvae [1, 4]. These receptors are essential for the efficacy of vector control programs targeting mosquitoes that transmit malaria, dengue, and Zika virus, though their effectiveness can be challenged by the development of resistance through receptor mutations [2, 4].
Toxin binding to specific receptors (APN, ALP, Cadherin) followed by oligomerization, membrane insertion, and pore formation, leading to osmotic lysis of midgut epithelial cells.
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