|Paldi, Nitzan -|
|Glick, Eitan -|
|Oliva, Maayan -|
|Zilbeberg, Yaron -|
|Aubin, Lucie -|
Submitted to: Applied and Environmental Microbiology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: December 1, 2010
Publication Date: March 20, 2010
Citation: Paldi, N., Glick, E., Oliva, M., Zilbeberg, Y., Aubin, L., Pettis, J.S., Chen, Y., Evans, J.D. 2010. Effective gene silencing of a microsporidian parasite associated with honey bee (Apis mellifera) colony declines. Applied and Environmental Microbiology. 76:5960-5964. Interpretive Summary: Colony collapse disorder and other factors are impacting honey bee health worldwide. One pathogen tied to bee declines is the gut parasite Nosema ceranae. Using insights from our genome project for this species, we designed and tested RNA controls, in collaboration with a company hoping to develop treatments for beekeepers. These controls were shown to be specific to Nosema genes, and they show great promise as a strategy to reduce this pest. Given that only one product is now available to control Nosema, this approach has great potential for aiding beekeepers in controlling an important disease.
Technical Abstract: Honey bee colonies are vulnerable to parasites and pathogens ranging from viruses to vertebrates. An increasingly prevalent disease of managed honey bees is caused by the microsporidian, Nosema ceranae. Microsporidia are basal fungi and obligate parasites with much reduced genomic and cellular components. A recent genome sequencing effort for N. ceranae indicated the presence of machinery for RNA silencing in this species, suggesting that RNA interference (RNAi) might be exploited to regulate Nosema gene expression within bee hosts. Here we use controlled laboratory experiments to show that double-stranded RNA homologous to specific N. ceranae ADP/ATP transporter genes can specifically and differentially silence transcripts encoding these proteins. This inhibition also affects Nosema levels and host physiology. Gene silencing could be mediated solely by Nosema or in concert with known systemic RNAi mechanisms in their bee hosts. These results are novel for the microsporidia and provide a possible avenue for controlling a disease agent implicated in severe honey bee colony losses. Moreover, since microsporidia are pathogenic in several known veterinary and human diseases, this advance may have broader applications in the future for disease control.