Mitochondria are the site of respiration in the cell and are essential for eukaryotic cell viability. Instability within the mitochondrial genome can result in loss of respiration, and is thought to contribute to a number of diseases such as diabetes mellitus, certain cancers and neuromuscular diseases, as well as other age-related diseases. The mitochondrial genome codes for proteins involved in oxidative phosphorylation and ATP production. Work in the lab centers on identifying genes from the RAD52 epistasis group involved in mitochondrial genome stability in the budding yeast, Saccharomyces cerevisiae. The RAD51 gene is a member of the RAD52 epistasis group whose members express key proteins required for the repair of DNA damage via recombination events. The RAD51 gene is essential for repairing damaged DNA, specifically, at sites of broken DNA. The protein, Rad51p, binds to the DNA at the site of a break and encases it in a protein sheath, which is an essential first step in the repair process. Its function is similar to the prokaryotic recA protein. Our lab has developed a series of genetic assays to determine the role of Rad51p in mitochondrial genome stability. In the absence of Rad51p, our preliminary data suggests that the rate of mitochondrial direct repeat-mediated deletion (DRMD) events was decreased 3-fold while observing a 6-fold increase in the nuclear DRMD rate. The lab is currently determining the effects loss of Rad51p has on cellular respiration and spontaneous point mutation within the mitochondrial genome. Fluorescence microscopy will also be performed to localize Rad51p to the mitochondria.
|Presenters:||Garry Coles (Graduate Student)
Rey Antonio Sia (Faculty)
|Time:||9:15 am (Session I)|