Garrett Prokosch, undergraduate researcher

Alaska INBRE Undergraduate Research Fellow, Sp10
A single residue in histone H2A, serine 122, is critical for the effective repair of all classes of DNA damage studied thus far. S122 is also vital for the maintenance of the histone-free mitochondrial genome, as mitochondrial function degrades rapidly in cells containing an alanine substitution at S122 (H2A-S122A). This is intriguing because the mechanisms responsible for maintaining and repairing the mitochondrial genome are quite different than those stabilizing the nuclear genome. It has been previously shown that H2A-S122A mutants are very sensitive to oxidative stress, a possibility being that increased reactive oxygen species (ROS) sensitivity causes mutant cells to actively down-regulate or degrade mitochondria, which are the primary source of intracellular ROS. Alternatively, increased ROS-dependent damage may directly lead to loss of mitochondrial DNA. This work will investigate whether oxidative damage plays a role in mitochondrial instability in H2A-S122A cells, seeing if increased ROS burden leads to loss of mitochondrial function in H2A-S122A cells.