Location: Bee Research LaboratoryTitle: Dicer regulates Nosema ceranae proliferation in honeybees
|HUANG, QIANG - UNIVERSITY OF BERN|
|LI, WENFENG - NON ARS EMPLOYEE|
|Chen, Yanping - Judy|
|RETSCHNIG-TANNER, GINA - UNIVERSITY OF BERN|
|YANEZ, ORLANDO - UNIVERSITY OF BERN|
|NEUMANN, PETER - UNIVERSITY OF CAMBRIDGE|
Submitted to: Insect Molecular Biology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 12/10/2018
Publication Date: 2/17/2019
Citation: Huang, Q., Li, W., Chen, Y., Retschnig-Tanner, G., Yanez, O., Neumann, P., Evans, J.D. 2019. Dicer regulates Nosema ceranae proliferation in honeybees. Insect Molecular Biology. 28(1):74-85. https://doi.org/10.1111/imb.12534.
Interpretive Summary: Nosema disease shortens the lifespan of worker honey bees and can make them more susceptible to pathogens and parasites. There are few management options for nosema. One strategy is to enhance natural honey bee defenses against this disease through breeding or management. This study describes an effort to temporarily silence an important protein in Nosema ceranae. This silencing results in a significant decrease in nosema spore loads and seems to trigger a range of changes in parasite health. This approach can be used as a feed treatment for honey bees to reduce disease and as a tool for better understanding Nosema biology. Reducing disease levels is a key goal in making honey bees available as important agricultural pollinators.
Technical Abstract: Nosema ceranae is a microsporidian parasite that infects the honeybee midgut epithelium. The protein-coding gene Dicer is lost in most microsporidian genomes but is present in N. ceranae. By feeding infected honeybees with small interfering RNA targeting the N. ceranae gene coding Dicer (siRNA-Dicer), we found that N. ceranae spore loads were significantly reduced. In addition, over 10% of total parasite protein-coding genes showed significantly divergent expression profiles after siRNA-Dicer treatment. Parasite genes for cell proliferation, ABC transporters and hexokinase were downregulated at 3 days postinfection, a key point in the middle of parasite replication cycles. In addition, genes involved in metabolic pathways of honeybees and N. ceranae showed significant co-expression. Furthermore, the siRNA-Dicer treatment partly reversed the expression patterns of honeybee genes. The honeybee gene mucin-2-like showed significantly upregulation in the siRNA-Dicer group compared with the infection group continually at 4, 5 and 6 days postinfection, suggesting that the siRNA-Dicer feeding promoted the strength of the mucus barrier resulted from interrupted parasite proliferation. As the gene Dicer broadly regulates N. ceranae proliferation and honeybee metabolism, our data suggest the RNA interference pathway is an important infection strategy for N. ceranae.