Abstract
Impairment in learning and memory behaviors in bees due to pesticide exposures and pathogen infections has resulted in massive disappearance of bee populations and subsequent agricultural economic losses. One of the causes of this bee colony collapse disorder (CCD) is the infection of deformed wing virus (DWV). The present study found that sodium butyrate, a histone deacetylase inhibitor (HDACi) previously shown to reverse the detrimental effects of a nicotine-like pesticide on learning behavior and memory in bees, significantly increased the survival of bee after DWV infection and reversed the learning/memory impairment in proboscis extension response (PER) assay. A next-generation sequencing analysis revealed the gene expression profile underwent DWV infection and sodium butyrate treatment and showed that sodium butyrate affected the expression of a wide range of genes involved in diverse biological processes. Particularly, sodium butyrate could up-regulate the expression of genes involved in glycolytic process and memory formation that were down-regulated during DWV infection. As brain physiological analyses presented that sodium butyrate restored the energy supply and the production of neurotransmitter in the infected bees, a large-scale movement tracking was performed by using a wireless sensor network (WSN)-based automatic real-time monitoring system and confirmed that sodium butyrate can improve the ability of DWV-infected bees to return to their hives. In short, we demonstrated the mechanism of how epigenetic regulation can resume the memory function of honeybees and suggested strategies for applying sodium butyrate as possible solutions for reducing the incidence of CCD.
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