Katy Gollahon

I am the laboratory manager for Peter Rabinovitch research group. I have been with the lab for about ten years, and I have lived in Seattle for twenty years. I did my graduate work in molecular biology at the University of Alabama in Birmingham and postdoctoral work at both the University of Washington and the University of Chicago. Since joining the lab, I have worked on a number of projects including work on Werner Syndrome, ulcerative colitis, Barrett's esophagus, and aging. I helped, in collaboration with Mike Shen and Jacintha O'Sullivan, to develop a protocol to evaluate telomere length in tissue. This work led to two publications one describing the relationship between epithelial telomeres length and progression to cancer in ulcerative colitis and the second one a techniques paper describing our methods for analyzing telomere length in tissue. Telomeres are the protective caps of DNA on the ends of chromosomes. With each cell division the telomeres within a cell shorten. At some point the short telomeres send a signal to the cells to senesce or stop dividing. Cells with short telomeres that continue to divide can undergo a phenomenon call "bridge breakage fusion" where the ends of the chromosomes fuse. When then cells tries to divide the chromosomes break creating two defective cells. Most defective cells will self-destruct through apoptosis, but an occasional defective cell survives and can undergo a second or third mutation. These mutated of cells put one at risk for the development of cancer. While this project took many years to complete it has been very satisfying to see that we can show that the biological phenomenon of telomere shortening can be used in predicting progression to cancer and that at some future date this analysis may be a useful clinical marker in screening patients at risk to develop colon cancer.

My current project concerns our studies with aging. As part of a program project we are studying the biology of aging. One of the parameters of aging we are examining is the role of oxidative stress in aging. Reactive oxygen species (ROS), for example hydrogen peroxide, are normal by products of cell metabolism. The cell has enzymes that convert the ROSs into inert substances. We have one mouse strain that has extra catalase, an enzyme that breaks down hydrogen peroxide. This mouse seems to live slightly longer than siblings without the extra enzyme. To explore this further, I am creating constructs that various other enzymes that also neutralize ROS. These constructs will be used to create transgenic mice that over express these enzymes. We hope that study of these strains of mice will broaden our understanding of oxidative stress in the context of aging.