期刊
SCIENTIFIC REPORTS
卷 7, 期 -, 页码 -出版社
NATURE PORTFOLIO
DOI: 10.1038/s41598-017-06623-z
关键词
-
资金
- National Sciences Foundation CAREER Program
- United States Department of Agriculture National Institute of Food and Agriculture, Agriculture and Food Research Initiative (USDA-NIFA-AFRI) Program
- Montana Department of Agriculture Specialty Crop Block Grant Program
- National Institutes of Health IDeA Program COBRE grant [GM110732]
- National Science Foundation [EPSCoR NSF-IIA-1443108]
- Hatch Multistate Funding [NC-1173]
- Project Apis m.
- Montana State Beekeepers Association
- Montana State University
- Montana State University Agricultural Experiment Station
- Project Apis m.-Costco Honey Bee Biology Fellowship
Recent high annual losses of honey bee colonies are associated with many factors, including RNA virus infections. Honey bee antiviral responses include RNA interference and immune pathway activation, but their relative roles in antiviral defense are not well understood. To better characterize the mechanism(s) of honey bee antiviral defense, bees were infected with a model virus in the presence or absence of dsRNA, a virus associated molecular pattern. Regardless of sequence specificity, dsRNA reduced virus abundance. We utilized next generation sequencing to examine transcriptional responses triggered by virus and dsRNA at three time-points post-infection. Hundreds of genes exhibited differential expression in response to co-treatment of dsRNA and virus. Virus-infected bees had greater expression of genes involved in RNAi, Toll, Imd, and JAK-STAT pathways, but the majority of differentially expressed genes are not well characterized. To confirm the virus limiting role of two genes, including the well-characterized gene, dicer, and a probable uncharacterized cyclin dependent kinase in honey bees, we utilized RNAi to reduce their expression in vivo and determined that virus abundance increased, supporting their involvement in antiviral defense. Together, these results further our understanding of honey bee antiviral defense, particularly the role of a non-sequence specific dsRNAmediated antiviral pathway.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据