Endochitinase from the Microsporidia Nosema ceranae facilitates infection in the honey bee Apis mellifera

Author:

da Cruz Souza Amanda Martins,Santos Carolina Gonçalves,Oliveira André Henrique,Carneiro Lenise Silva,Resende Matheus Tudor Cândido Santos de,Oliveira Leandro Licursi,Serrão José Eduardo

Abstract

AbstractBees are crucial pollinators in terrestrial ecosystems, responsible for 80% of insect-driven pollination and playing a vital role in the pollination of 75% of crops. The honey bee, Apis mellifera, is not only used in honey production but also serves as a pollinator in agriculture. However, A. mellifera faces various challenges, including exposure to pathogens such as the Microsporidia Nosema ceranae, which has been linked to decreased crop yields and colony losses. Nosema ceranae spores infect adult honey bees by penetrating the midgut lumen and invading the cytoplasm of epithelial cells, completing their life cycle. However, the midgut possesses a protective mechanical barrier called the peritrophic matrix, composed of chitin and proteins, which prevents epithelial infection. Nevertheless, N. ceranae overcomes this primary defense mechanism, though the specific mechanisms it employs to cross the peritrophic matrix and reach the midgut epithelium are not yet well understood. This study aimed to investigate the potential role of the predicted endochitinase from N. ceranae to infect bees. We tested the hypothesis that inhibiting the expression of N. ceranae endochitinase through RNA interference would impact the pathogen infection of A. mellifera. Bees treated with dsRNA targeting endochitinase, administered 12 and 24 h after spore inoculation, exhibited suppressed endochitinase gene expression and a decrease in the number of total and viable N. ceranae spores in the midgut. These results indicate that inhibiting the expression of the target gene through RNA interference affects Microsporidia infection, underscoring the importance of this enzyme in the infection process.

Publisher

Springer Science and Business Media LLC

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