1. What is your lab’s long-term/big-picture research goal?
The long-term goal of our lab is to understand how cells protect DNA from double-strand breaks. DNA double-strand breaks affect our cells daily. They are caused and repaired by normal cellular processes. If just one double-strand break is left unrepaired, it can result in cell death or cancer. We are trying to understand the mechanisms that allow for efficient double-strand break repair.
2. What is your training/scientific background?
I received my Bachelor of Science degree in Biology from The University of Texas at Austin. During this time, I worked in the lab of Dr. G. Barrie Kitto on the development of novel therapies designed to eliminate HIV infected T cells to help treat AIDS patients. After receiving my degree, I went on to receive my Ph.D. in the lab of Dr. Phillip B. Carpenter at the University of Texas Health Science Center in Houston. That is where my interest in understanding double-strand break repair began. I used a mouse model to understand the function of the DNA damage regulator 53BP1 and its role as a tumor suppressor. After my Ph.D. work, I went to the University of Texas Southwestern Medical Center to do my postdoctoral work . I continued working on understanding how DNA double-strand breaks are repaired, with an emphasis on double-strand breaks generated by transcription. Then I was recruited as an Assistant Professor to OUHSC, where my lab continues to try and understand how the cell repairs transcription-mediated double-strand breaks.
3. What is the goal of your OCASCR project?
Induced pluripotent stem cells (iPSCs) hold great potential for the treatment of a variety of diseases. We know that these cells undergo a lot of transcription, which makes them susceptible to double-strand breaks. If left uncorrected, DNA breaks can result in cell death or changes in the genome that could be dangerous for the patient ultimately receiving the cells. Our studies are targeted toward trying to understand how stem cells repair double-strand breaks and avoid these deleterious effects.
4. How might your research impact diseases related to obesity or smoking?
Smoking and obesity put undue stress on the body. Smoking also introduces substances into cells that directly introduce DNA damage. Understanding how this damage is repaired could allow us to prevent disease.
5. What’s your most critical piece of research equipment in your lab? Why?
The most important piece of equipment is the Cytation5 imaging station. This microscope allows us to visualize and monitor the formation of DNA damage, along with its repair. We have been able to visualize how manipulation of transcription regulators affects double-strand break formation and repair in iPSCs.
6. What’s your favorite scientific meeting to attend? Why?
My favorite scientific meeting to attend is the annual meeting of the Radiation Research Society. This meeting brings together experts in the DNA damage field and allows us to share our findings with one another. In addition, the location is typically some place nice, such as Hawaii or Las Vegas.
7. What started my interest in DNA and DNA damage?
I was 13 years old and a freshman in high school. My biology teacher at the time showed us the movie “The Race for the Double Helix.” Then we went on to extract DNA from plant cells and bacteria. I was amazed at how so much DNA could fit in a cell and was eager to understand more about it.
