Our studies of the honey bee’s cellular stress responses aim to increase understanding at various levels, including the colony, the individual bee, the cell, and the molecular pathway. As a social insect, the honey bee provides a unique opportunity to examine ways in which group resistance is affected by individual stress responses. Increased knowledge about how honey bees sense and attempt to adapt to these stresses at the cellular level will be important for understanding diseases affecting this crucial beneficial insect. In the realm of immunity in particular, our studies have significant potential implications for understanding the spread of human disease.


Infectious disease and immune activation: 

Among the environmental stressors implicated in honey bee disease, there has been intensifying focus on the role of microbial attack on honey bee health. Since the advent of the phenomenon known as Colony Collapse Disorder in 2006, significant emphasis has been placed on the possibility that novel microbial pathogens might be largely to blame for honey bee colony deaths. The hunt for emerging infectious agents has been extensive and produced truly remarkable advances in our understanding of the types, levels, and community architecture of pathogenic and non-pathogenic microbes associated with honey bees and their hives. Increasing our understanding of how honey bees sense and defend against infection is critical to complement the microbial studies above. To that end our lab has developed models for infection for multiple microbes, identified a novel infectious agent, and begun characterization of gut barrier immunity. 

Proteotoxic stimuli: 
As no single cause for the recent increase in honey bee disease is evident, there is increased focus on the impact of interactions between various stressors. A critical first step in understanding these synergies involves defining specific common cellular processes that are impacted by multiple stressors and could therefore serve as links to cellular dysfunction, tissue pathology, disease, and mortality in honey bees. The various pathways that make up cellular stress responses provide logical and compelling processes to examine for such interactions. One critical cellular stress involves problems in proteostasis, which refers to the homeostasis of protein synthesis, folding, function, and degradation both within a cell and in an organism as a whole. A number of normal and pathologic conditions can lead to disruption of proteostasis, leading to a build-up of unfolded proteins in the cell and triggering a suite of responses designed to limit damage to the cell from problems in protein folding and return the cell to homeostasis. Within individual cells, proteostasis is maintained by the responses of the proteostatic network, including the Heat Shock Response (HSR), responding to proteostatic disruption in the cytoplasm, and the Unfolded Protein Response (UPR), responding to proteostatic perturbation in the endoplasmic reticulum (ER). Notably in other organisms, these pathways have been shown to influence cellular and organismal outcomes to exposures to the very environmental stressors suspected of playing a part in recent honey bee losses, including parasitic and microbial attack, nutritional stress, and chemical toxicity. However, the UPR and HSR have not been completely characterized at the molecular level in honey bees. In two projects, we have provided the foundational characterization of these pathways and begun to investigate their role in honey bee health and disease.

Microsporidia Infection:

Microsporidia are obligate intracellular parasites that that cause widespread infections in nature, but are relatively understudied compared to microbial pathogens representing other taxonomic groups, such as bacteria and non-microsporidial fungi. These pathogens infect diverse species that play important roles throughout our food production system as well as causing disease in immunocompromised humans. Nosema ceranae is a microsporidian species that infects the honey bee midgut and can cause individual mortality and contribute to colony collapse. While most microsporidia infection can currently be controlled by treatment with the drug Fumagillin, high doses of this drug are toxic to host cells and the potential for development of resistance suggests the need for alternative treatment strategies. In addition, no easy, cheap, and reliable field test for Nosema infection exists, causing Fumagillin to be administered regardless of the presence or absence of infection. Our lab seeks to advance our understanding of the cell biology of N. ceranae to help address these problems in controlling this infectious agent in honey bee disease. In addition, we hope to apply new knowledge to microsporidian infections more broadly with potential impact food production and human health.

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