Location: Bee Research LaboratoryTitle: Silencing honey bee naked cuticle (nkd) reduces Nosema ceranae replication and disease levels Author
|Li, Wenfeng - Zhejiang University|
|Huang, Qiang - University Of Bern|
|Rodriguez, Cristina - Bee Pathology Laboratory And 2hive Products Laboratory|
|Liu, Jie - Fujian Agricultural & Forestry University|
|Grozinger, Christina - Pennsylvania State University|
|Webster, Thomas - Kentucky State University|
|Su, Songkun - Fujian Agricultural & Forestry University|
|Chen, Yanping - Judy|
Submitted to: Applied and Environmental Microbiology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 9/20/2016
Publication Date: 12/3/2016
Citation: Li, W., Evans, J.D., Huang, Q., Rodriguez, C.G., Liu, J., Hamilton, M.C., Grozinger, C.M., Webster, T.C., Su, S., Chen, Y. 2016. Silencing honey bee naked cuticle (nkd) reduces Nosema ceranae replication and disease levels . Applied and Environmental Microbiology. 82(22):6779-6787.
Interpretive Summary: Given the critical role of honey bees in the pollination of agricultural crops, it is urgent to develop strategies to prevent the colony decline induced by the infection of parasites/pathogens. Here, we demonstrate that knocking down a honey bee immune suppressor using a novel technology called RNAi can suppress the reproduction of the honey bee parasite Nosema and improve the overall health of honey bees. To the best of our knowledge, this is the first success in designing an effective therapeutic to control pathogenic infection of honey bees by focusing on a host immune suppressor. The information obtained from this study will have positive implications for honey bee disease management and breeding practices.
Technical Abstract: Nosema ceranae is a new and emerging microsporidian parasite of European honey bees, Apis mellifera that has been implicated in alarming colony losses worldwide. RNA interference (RNAi), a post-transcriptional gene silencing mechanism, has emerged as a potent and specific strategy for controlling infections of parasites and pathogens in honey bees. While previous studies have focused on the silencing of parasite/pathogen virulence factors, the present study used an RNAi strategy to mitigate the N. ceranae infection by repressing the expression of a honey bee host gene, naked cuticle (nkd), which is an inducible antagonist of the Wnt signaling pathway. While nkd mRNA levels in adult bees were upregulated by N. ceranae infection, the ingestion of dsRNA specific to nkd could efficiently silence its expression. Furthermore, our study showed that knockdown of the gene for nkd in Nosema-infected bees could lead to the upregulated expression of immune genes, Abaecin, Apidaecin, Defensin-1, and PGRP-S2, reduction of Nosema spore loads, and extension of honey bee lifespan. The results of our studies clearly indicate that silencing the host nkd gene can activate honey bee immune responses, suppress the reproduction of N. ceranae and improve the overall health of honey bees. This study represents a novel host-derived therapeutic for honey bee disease treatment that merits further exploration.