Does Rad6 regulate the quantity and function of yeast mitochondria as an adaptive response to oxidative stress?

Sofia Guerrero

Mentors: Vanessa Simões, Gustavo Silva, Ph.D.

Department of Biology

Oxidative stress, where cells accumulate reactive oxygen species (ROS), is among the most prominent types of harmful environment, damaging cellular biomolecules, fostering cell death, and contributing to neurodegeneration. Cells experience many endogenous and exogenous sources of ROS; however, mitochondria are one of the largest contributors. Functional mitochondria are important for neural and muscle tissue, which require large amounts of energy for proper function. Moreover, defective mitochondria are associated with several human diseases, including Alzheimer’s, Parkinson’s, and muscular dystrophy. Despite this, the mechanisms impacting mitochondrial function in response to oxidative stress are not fully understood. This study aims to elucidate the key role of a ubiquitin enzyme Rad6 in the regulation of yeast mitochondrial function. Through biochemical and fluorescent imaging methods, we demonstrated that deletion of RAD6 increases the number and function of mitochondria. These mitochondria are required for cellular growth as rad6Δ cells become more susceptible to mitochondria targeting drugs. Through further investigation, we will test whether Rad6 regulates the quantity and activity of mitochondria as an adaptive response to the harmful effects of oxidative stress.

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