Heme Trafficking Under Lead Stress in S. Cerevisiae

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Hu, Rebecca A.
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Heavy metals, including lead, are significant for their toxicity to the environment and to organisms’ physiology. Lead has been shown to induce oxidative stress in cells through mitochondrial perturbation, as well as affecting heme homeostasis. The initial hypothesis was to study heme as an interorganellar signaling molecule in S. cerevisiae cells using a novel genetically encoded fluorescently heme sensor, specifically as a mitochondrial retrograde signaling molecule. In addition to labile and total heme measurements, growth and changes in the protein profile were also assessed to determine how lead affects the cells’ viability and stress response. It was found that there was no significant evidence of mitochondrial retrograde signaling with the labile heme pool, but that there was a preservation of the labile heme pool despite a marked decrease in total heme under lead conditions. The results support a model in which high affinity hemoproteins such as catalase are degraded under lead stress, while lower affinity ones such as glyceraldehyde phosphate dehydrogenase (GAPDH) are maintained. These results will help shape the understanding of the presence and purpose of the labile heme pool and how cells respond to oxidative stress in the context of heme.
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Undergraduate Thesis
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