Lab Members

Paul W. Doetsch, PhD
Cheryl Clauson
Dan Swartzlander
Lydia Morris
Nick Bauer
Jordan Moreall
Natasha Degtyareva, PhD
Paula Wardlaw
Stacy Holloway, CRA
Tina Saxowsky, PhD

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Paul W. Doetsch, Ph.D., is Professor of Biochemistry, Radiation Oncology and Hematology & Oncology and is the Emory University School of Medicine Distinguished Chair in Cancer Research; For several years he served as Interim Associate Director for Basic Research and since January, 2005 (following a National search) has been Deputy Director for Basic Research at the Winship Cancer Institute. Dr. Doetsch obtained his doctoral training in nucleic acids biochemistry in the laboratory of Dr. Robert Suhadolnik at Temple University School of Medicine. He then conducted postdoctoral work as a NIH NRSA recipient at the Dana Farber Cancer Institute, Harvard Medical School in the laboratory of Dr. William Haseltine. Dr. Doetsch has been a faculty member engaged in basic cancer research at Emory since 1985. He has been associated with the Winship Cancer Institute and the leadership and development of its scientific programs for many years. He is the Program Director of a Program Project Grant, “Cellular Responses to Genotoxic Stress” and has a long track record of RO1 grant support from the NCI. Dr. Doetsch has served in the past as a regular member of the Radiation Study Section at the NIH and the Carcinogenesis, Nutrition and Environment study section of the American Cancer Society. He is internationally recognized for his studies and publications in the areas of DNA damage repair, mutagenesis and genetic instability. Over a decade ago, he discovered transcriptional mutagenesis and has been a pioneer in this area and its leading authority. He is the co-editor of a recent (2006) textbook, “DNA Damage Recognition” and has trained dozens of Ph.D. students and postdoctoral fellows. He serves on several important School of Medicine advisory committees, including the Research Advisory Council (RAC). (back to top)

Cheryl Clauson - Graduate Student
Genetics and Molecular Biology
Research: Most cells in nature that are exposed to DNA damaging agents are not undergoing continuous rounds of replication, but are frequently engaged in transcription. Therefore, it is important to understand the nature of RNA polymerase (RNAP) encounters with DNA damage, and the resulting biological consequences. If the transcription machinery bypasses some lesions, as has been shown in vitro for smaller, spontaneously occurring damages, this can lead to a population of mutant mRNAs, and mutant protein production, a process we have termed transcriptional mutagenesis (TM). TM may have biological importance in bacteria as a strategy to adapt to stressful environments. TM could also be important in mammals, as a route for generating mutant proteins, as most cells in tissues are not undergoing continuous cycles of DNA replication and cell division. It is possible that TM could have roles in human diseases such as cancer or prion-based neurodegenerative conditions.

We are using a luciferase reporter assay in E. coli to study which DNA repair pathways influence TM caused by the small, spontaneous lesions, uracil and 8OG, in bacteria. Also, we are using the yeast S. cerevisiae to examine whether transcriptional mutagenesis can lead to the formation of prions, specifically through TM occurring in a critical location of the sup35 gene, a known prion-causing gene in yeast. (back to top)

Dan Swartzlander - Graduate Student
Genetics & Molecular Biology
Research:  Understanding how the cell responds to threats to its DNA from oxidative stress and other DNA damaging agents is important in determining how an organism is able to protect itself from cancer and other neurodegenerative diseases.  Accumulation of reactive oxygen species (ROS), which are produced and primarily found in the mitochondria, leads to a state of oxidative stress in the cell and causes DNA damage.  The base excision repair (BER) pathway, which repairs small DNA lesions such as those induced by ROS, has been shown to be involved in repair of both nuclear and mitochondrial DNA.  In order to efficiently protect its DNA, either nuclear or mitochondrial, the cell needs to prioritize where its DNA repair enzymes are allocated.  The protein Ntg1p which is involved in the recognition of damaged bases and has both N-glycosolase and AP lyase function has been shown through previous work in the lab to localize to both the nucleus and mitochondria where it is involved in BER.  I am interested in determining how the localization of Ntg1p is effected by oxidative stress on both the entire cell and in the mitochondria alone and in determining what proteins may be involved in sensing this stress state responsible for reallocating Ntg1p.

Lydia Morris - Graduate Student
Genetics and Molecular Biology
Research Project: We are interested in studying the base excision repair (BER) pathway in yeast. The basic biochemical steps of this BER are highly conserved, thus our findings will be applicable to humans. In particular, we wish to map the genomic localization of the yeast major AP endonuclease, Apn1. This will reveal how the cell prioritizes localization to damage by proteins that are expressed at very low levels in the cell. To gain more insight, we will also use different genetic backgrounds as well as exogenous mutagens such as H 2O 2. Studying this and other pathways will help us to better understand how DNA repair contributes to genomic instability, an important component of tumorigenesis. (back to top)

Nick Bauer - Graduate Student

Research Project:

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Jordan Morreall - Graduate Student

Research Project:

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Natasha Degtyareva, PhD - Assistant Professor
Research Project: The main goal of my research project is to understand the mechanisms that maintain eukaryotic genome stability. I study different cellular systems that play key roles in the maintenance of the eukaryotic genome: DNA replication, recombination, and repair using  Saccharomyces cerevisiae. (back to top)

Paula Wardlaw - Senior Program Associate
Mini Bio: Upon moving to Atlanta, I joined Emory's DNA Core Facility working in the Affymetrix GeneChip lab in March 2002 and moved to the Doetsch lab in November the same year. As a research technician, I worked on understanding the role of the Alternative Excision Repair (AER) pathway in S. pombe in the repair of DNA damage caused by anti-cancer drugs. Later projects explored genomic instability due to double strand breaks and chromosome arm loss in S. cerevisiae. In February 2005, I took on an administrative role as a Program Associate with Dr. Doetsch and the Emory Winship Cancer Institute. In this position, I coordinate the activities of the shared resources committee as well as help with the administrative duties of the Associate Director for Basic Research. I also work with website design for Dr. Doetsch's laboratory activities. (back to top)

Stacy Holloway, CRA - Senior Research Project Coordinator
Mini bio: As a registered Radiologic Technologist, I spent ten years as a Radiographer and then eight years as the Patient Care Coordinator for Interventional Radiology at Emory University Hospital. I was the Patient Relations Coordinator for Emory Healthcare for two years before joining Dr. Doetsch as the Project Administrator for the NIEHS Program Project Grant "Investigation of cellular Responses to Genotoxic Stress." (back to top)

Tina Saxowsky, PhD - Postdoctoral Research Associate
Research: It has been previously shown, primarily in bacteria and phage, that some of the most commonly occurring types of cellular DNA damage (for example,  uracil and 8-oxoguanine) are readily bypassed by RNA polymerase when in the  template strand during transcription. Additionally, these lesions have miscoding  properties, leading to a population of mutant mRNAs with potential to code for  mutant proteins that could influence the phenotype of the cell. This process is  known as transcriptional mutagenesis (TM). The major goal of my project is to  develop a mammalian cell culture system within which to investigate TM with  application to a biologically relevant endpoint. I am examining the potential role of  TM in the expression of a mutant Ras protein as a critical event in cancer  development. (back to top)