You are hereHome › University of Toledo Student Research › Humanity First Research Symposium Archive › How Cells Cope with Stress Style American Medical Association (JAMA)APAChicago 16 - author-dateChicago 17IEEEModern Language Association (MLA)National Library of Medicine Choose the citation style. Search for this publication on Google Scholar Acharya, A., Manivannan, P., Hibbard, B., Ramnani, B., Kesterson, S., & Krishnamurthy, M. (2020). How Cells Cope with Stress. Humanity First Research Symposium 2020. How Cells Cope with Stress Details Title How Cells Cope with Stress Contributor(s) Acharya, Aditya (author)Manivannan, Praveen (author)Hibbard, Brian (author)Ramnani, Barkha (author)Kesterson, Shelby (author)Krishnamurthy, Malathi (author) Located In Humanity First Research Symposium 2020 Date 2020 Abstract The goal of this project is to understand how cells combat stress. This research will add to the current information the scientific community has on the role of stress granules. Stress granules are formed in response to the many stresses prevalent in the cell. In the body, there are many forms of stress that cells experience. I will be focusing on stress granules induced by heat shock and oxidative stress. To trigger stress granule formation, translation of messenger RNAs must come to a halt. When this happens, key stress granule protein such as G3BP1 aggregate together and form stress granules. The first aim is to generate stable cell lines expressing GFP-G3BP1 plasmid. Whereas in the stable cell line we can monitor G3BP1 activity live in cells, to monitor endogenous G3BP1 activity we use the immunofluorescence technique. In order to track G3BP1 activity we must treat cells with hydrogen peroxide (H2O2) or Heat shock and determine the optimal timepoints and concentrations of the stressors that trigger stress granule formation. For the H2O2 treatments, monitoring both endogenous and over-expressed GFP-G3BP1, I examined several fields for each treatment to determine the percent of cells forming stress granules per treatment. With varying concentration of H2O2 and by monitoring endogenous G3BP1 localization, I found that at 2 mM and 3 mM of H2O2, there was the highest percent of cells forming stress granules. Through monitoring endogenous and overexpressed G3BP1 activity, we were able to determine that 2 mM/3mM and 3 hours of H2O2 were optimal for inducing stress granule formation. In future studies, we will be inducing stress granules using heat shock and monitor stress granule formation at different temperature. Stress granules aggregate most of the proteins required for translation within cell to reduce energy being consumed as well as preventing unregulated translation. This project adds to current research by conducting experiments that determine how cells cope with very specific stresses such as oxidative stress and heat shock. By understanding these mechanisms, I hope to further understand the role of stress granules during viral infections.