Deletion of Skn7 and Yap1 Reduces Delayed Oxidative Stress Responses in Saccharomyces cerevisiae

Abstract:

In this experiment we removed two genes from yeast cells, Yap1 and Skn7, to identify their affect in the pathway responsible for oxidative stress response. Oxidative stress is a result of oxygen metabolism and the buildup of reactive oxygen species. Reactive oxygen species can damage important biological processes by oxidizing lipids, DNA proteins, lipids, and nucleic acids, causing a decrease in enzyme efficiency, protein function, fluidity of membranes, reduced gene expression, and inhibits anabolic processes in the cells. Reactive oxygen species activate two pathways required for defending against oxidative stress. These pathways stop reversible nonessential functions, inhibiting protein synthesis, focusing on antioxidant defenses. One pathway is essential for immediate oxidative stress response, the other for delayed oxidative stress response. The Yap1 and Skn7 genes are both located in quick oxidative stress response. Unlike any research done previously we tested the effects of single and double deletions of Yap 1 and Skn7 in the opposite pathway from which they are located. We performed a cross to create the double deletion then we used reporter assay to observe the cell response. For our experiment our hypothesis was that the two pathways are both independent of each other, due to their separate activation. If the two pathways are independent, then the single and double deletion of Yap1 and Skn7 will have no effect delayed oxidative stress. Our preliminary results proved our hypothesis incorrect suggesting that the Yap1 pathway may influence delayed oxidative stress response, and they are not as independent as they seem.