Kenneth R. Peterson, PhD
Professor Peterson received his undergraduate training at Northern Arizona University, Flagstaff where he received a B.S. degree in Microbiology and Chemistry in 1979. He received a M.S. in Microbiology and Biochemistry in 1981. In 1987, Professor Peterson completed his Ph.D. degree in Molecular and Cellular Biology at the University of Arizona, Tucson. From 1987 to 1990, he received postdoctoral training in molecular evolution at the University of Arizona, Tucson. Additional postdoctoral training in human genetics and molecular biology was obtained at University of Washington, Seattle. In 1992, Professor Peterson was appointed as a Research Assistant Professor in the Division of Medical Genetics, Department of Medicine at the University of Washington. He was promoted to Research Associate Professor in 1996. In 1998 Dr. Peterson moved to the University of Kansas Medical Center as an Associate Professor and was promoted to the position of Professor of Biochemistry and Molecular Biology in 2003. In 2003, he also was appointed Vice Chair of the Department of Biochemistry and Molecular Biology.
Professor Peterson is internationally recognized for his novel and innovative scientific achievements in the field of developmental genetics, gene regulation and epigenetics. His laboratory is actively investigating mechanisms underlying the control of hemoglobin synthesis and blood cell formation.
For the past 26 years, Professor Peterson’s research has been supported largely by the NIH and has resulted in the publication of 103 manuscripts. Dr. Peterson has served on NIH Study Sections and as a reviewer for numerous journals. He has been honored with a Madison and Lila Self Graduate Fellowship Faculty Scholar Award for research and mentoring in 2001, recognized for his research on globin gene switching by the University of Kansas School of Medicine with a Faculty Investigator Research Award in 2003 and the Chancellor’s Club Research Award in 2015, and named a Fulbright Scholar in 2009. Professor Peterson has also directly supervised the training of both postdoctoral fellows and three graduate students during his career.
Education and Training
- BS, Microbiology & Chemistry, Northern Arizona University
- MS, Microbiology, Idaho State University
- PhD, Molecular Biology, University of Arizona
- Other, University of Arizona
- Post Doctoral Fellowship, Molecular Genetics, University of Washington, Seattle, WA
Red blood cells (RBCs) carry oxygen to tissues and organs and ferry waste carbon dioxide back to the lungs for exhalation. Hemoglobin is the molecule in RBCs responsible for this transport and is comprised of two a-like globin chains, two b-like globin chains and four heme molecules. Diseases of RBCs, termed hemoglobinopathies, include sickle cell disease (SCD) and b-thalassemias. SCD affects RBC shape and renders them ineffective; resulting in anemia along with attendant complications. SCD is caused by a single point mutation in the coding sequence of the adult b-globin gene. b-thalassemias also cause anemia and result from an array of mutations in the b-globin locus that affect b-globin gene function. By understanding the molecular mechanisms underlying these diseases, targeted drug treatments or gene therapies will be developed to treat these disorders.
The human b-globin locus consists of five functional b-like globin genes, all of which serve as the b-chain in the hemoglobin molecule during different stages of development. Reactivation of the fetal b-like globin genes, the g-globin genes, in adults to treat SCD or certain b-thalassemias is widely accepted as the most effective treatment for these diseases and is an important line of active research in the hematology field. Introduction of a g-globin gene into adult blood stem cells to substitute for the defective adult b-globin gene or correcting the underlying genetic defect by genome editing are current gene therapy goals. Achieving these milestones requires understanding the molecular mechanisms that regulate globin gene switching. We are focused on the cis- and trans-control of human b-like globin gene expression during development. Specific cis-regulatory sequences under study include the locus control region (LCR), chromatin domain boundary elements, and g-globin gene silencers. We also study 1) g-globin-specific transcriptional co-activators and co-repressors and the function of a non-coding RNA on globin gene switching; 2) we are analyzing pharmacologic g-globin inducers identified in a high-throughput drug screen; and 3) we are using a cell-based selection to collect all possible mutations that result in up-regulation of g-globin gene expression. More recently, we are analyzing the role of the O-GlcNAc post-translational modification in regulating erythropoiesis and globin gene switching. Novel experimental systems include transgenic mice and derivative bone marrow cells produced with human b-globin locus yeast artificial chromosome (b-YAC) transgenes. We use a variety of cutting-edge molecular biology/genetics and biochemistry techniques to study cis-regulation, protein-DNA, and protein-protein interaction during development using these models.