PLoS Pathog. 2026 Aug 17;22(8):e1014521. doi: 10.1371/journal.ppat.1014521. Online ahead of print.
ABSTRACT
Microsporidia rely extensively on host resources, yet how parasite-derived microRNAs coordinate infection remains poorly understood. Here, we investigated the function of nce-miR-12220, a miRNA identified in Nosema ceranae spores, during infection of Apis mellifera workers. Target prediction, dual-luciferase assays, and fluorescence in situ hybridization were combined with RNA interference and miRNA gain- and loss-of-function experiments. nce-miR-12220 interacted sequence-specifically with binding regions in ATP-A and γ-tubulin and was detected in infected honeybee midgut epithelial cells. Silencing either target gene reduced expression of the N. ceranae virulence-associated gene NcRBL and improved worker survival relative to the scramble control. In infected workers, nce-miR-12220 overexpression increased endogenous ATP-A and γ-tubulin transcript abundance, whereas inhibition produced the opposite effect. Overexpression also reduced expression of the Toll pathway-associated genes Cactus and dorsal and the antimicrobial peptide genes Defensin and Hymenoptaecin, increased N. ceranae spore load and sucrose consumption, and decreased midgut ATP content. Inhibition of nce-miR-12220 reversed these responses and reduced parasite burden. Survival after nce-miR-12220 manipulation changed in the predicted direction but did not reach statistical significance. Together, these findings identify nce-miR-12220 as a parasite-derived regulator that promotes N. ceranae proliferation while reshaping host immune and energetic responses, and suggest that this microRNA and its target network may provide candidates for controlling bee nosemosis.
PMID:42607084 | DOI:10.1371/journal.ppat.1014521
