- Rey Sia Ph.D.
- Associate Professor and Chair
- email: email@example.com
- Lennon Hall, Room 215, Tel: 395-2783
The current research in my lab centers around the mechanism of DNA repair. Using modern molecular and genetic techniques, work in the lab focuses on the identification of nuclear-encoded proteins that regulate the stability of the mitochondrial genome in the budding yeast, Saccharomyces cerevisiae.
The long-term goal of our research is to identify the molecular pathways that ensure the integrity of the mitochondrial genome. A functional mitochondrial genome is essential for the survival of eukaryotic cells. A number of inherited neurodegenerative disease syndromes arise as a result of mitochondrial mutation, demonstrating the profound importance of a functional mitochondrial genome to human health. Deletions of the mitochondrial genome are easily detected and have been found in a variety of tissue types in aging mammals. Spontaneous mtDNA deletions are often flanked by identical or nearly identical repeats. To examine how such deletions arise, we have developed a system for monitoring direct-repeat mediated deletions (DRMDs) in the mitochondrial genome of the budding yeast, Saccharomyces cerevisiae. Using genetic assays involving our DRMD reporters, we have identified a number of genes of the double-strand break repair pathways whose products impact the rate at which these deletions occur. In addition, the homologs of some of these proteins have been found in mitochondria purified from mammalian cells, suggesting the conservation of some of these pathways between yeast and vertebrates.
The three specific research aims of the lab are: i) to identify the factors that repair directed mitochondrial double-strand breaks (DSBs), ii) to analyze the protein complexes responsible for mitochondrial DRMD, and iii) to directly compare the rates of nuclear and mitochondrial DRMD.