Faculty Sponsor(s)
Megan Bestwick
Subject Area
Chemistry
Description
Superoxide is a reactive oxygen species (ROS) produced by premature electron leakage from complexes of the electron transport chain directly to oxygen. A primary defense of ROS damage as a respiratory byproduct is the neutralization of the superoxide anion by the enzyme Superoxide dismutase 1 (Sod1) to the less harmful hydrogen peroxide molecule. ROS are harmful species that cause degradation of proteins and membranes like the cell well, as well as mutations to DNA. The Sod1 protein requires copper and zinc as cofactors in the conversion of superoxide to less harmful hydrogen peroxide. Copper plays an important role in yeast cell growth and mitochondrial activity, and addition of non-toxic levels of copper sulfate to media increases the yeast lifespan of wild type cells as determined by the chronological lifespan assay.
Mutations in the Sod1 protein have also been linked to the development of Amyotrophic Lateral Sclerosis, or ALS, which is a degenerative disease affecting the function of muscles within the body. To strengthen the mechanistic understanding and connection between Sod1 and the development of ALS, we aim to determine the effect on yeast lifespan of the amyotrophic lateral sclerosis (ALS) mutation G93A in Sod1 and resulting effect of copper supplementation at non-toxic levels in the presence of the mutation. Yeast are used as a model organism for this study due to the similarity of the yeast protein to the human protein.
Recommended Citation
Harrison, Devin J. R., "Role of Superoxide Dismutase 1 (Sod1) in Yeast Lifespan and Model for ALS" (2026). Linfield University Student Symposium: A Celebration of Scholarship and Creative Achievement. Event. Submission 26.
https://digitalcommons.linfield.edu/symposium/2026/all/26
Role of Superoxide Dismutase 1 (Sod1) in Yeast Lifespan and Model for ALS
Superoxide is a reactive oxygen species (ROS) produced by premature electron leakage from complexes of the electron transport chain directly to oxygen. A primary defense of ROS damage as a respiratory byproduct is the neutralization of the superoxide anion by the enzyme Superoxide dismutase 1 (Sod1) to the less harmful hydrogen peroxide molecule. ROS are harmful species that cause degradation of proteins and membranes like the cell well, as well as mutations to DNA. The Sod1 protein requires copper and zinc as cofactors in the conversion of superoxide to less harmful hydrogen peroxide. Copper plays an important role in yeast cell growth and mitochondrial activity, and addition of non-toxic levels of copper sulfate to media increases the yeast lifespan of wild type cells as determined by the chronological lifespan assay.
Mutations in the Sod1 protein have also been linked to the development of Amyotrophic Lateral Sclerosis, or ALS, which is a degenerative disease affecting the function of muscles within the body. To strengthen the mechanistic understanding and connection between Sod1 and the development of ALS, we aim to determine the effect on yeast lifespan of the amyotrophic lateral sclerosis (ALS) mutation G93A in Sod1 and resulting effect of copper supplementation at non-toxic levels in the presence of the mutation. Yeast are used as a model organism for this study due to the similarity of the yeast protein to the human protein.