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Kenneth Peterson
Professor
- Department of Biochemistry and Molecular Biology
- University of Kansas Medical Center
- 913-588-6907
kpeterson@kumc.edu
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Education and Experience
- Northern Arizona University, B.S., Microbiology, Chemistry, 1979
- Idaho State University, M.S., 1981
- University of Arizona, Ph.D., 1987
- University of Washington, Seattle, Washington, Research Assistant Professor of Medicine,
Division of Medical Genetics, Department of Medicine, 1992-1996
- University of Washington, Seattle, Washington, Adjunct Research Assistant Professsor of
Genetics, Department of Genetics, 1996
- University of Washington, Seattle, Washington, Adjunct Research Associate Professor of
Medicine, Division of Medical Genetics, Department of Mediciine, 1996-1998
- University of Washington, Seattle, Washington, Adjunct Research Associate Professor of
Genetics, Department of Genetics, 1996-1998
- University of Kansas Medical Center, Kansas City, Kansas, Associate Professor of
Biochemistry and Molecular Biology, Department of Biochemistry and Molecular Biology,
1998-present
- University of Kansas Medical Center, Kansas City, Kansas, Associate Professor of Anatomy
and Cell Biology, Department of Anatomy and Cell Biology, 1998-present
Major Research Interests
My major interest is genetic regulatory mechanisms with emphasis on the delineation of
the function of locus control regions (LCRs). The human beta-globin locus serves as our
primary model system. This locus consists of 5 functional genes arrayed in their order of
expression during development, 5'-epsilon-Ggamma-Agamma-delta-beta-3'. The LCR is located
6- to 20-Kb upstream of the epsilon-globin gene. It is composed of five
DNAseI-hypersensitive sites (HSs), which are highly conserved during evolution. The globin
LCR has multiple properties, including the activation and maintenance of open chromatin
domains, insulation from the effects of surrounding negative chromatin, conference of
erythroid cell lineage specificity on globin gene expression and enhancement of globin
gene transcription. LCRs or LCR-type elements have been identified in over 30 mammalian
loci, but they are less understood compared to the beta-globin locus LCR. The mechanism of
action of the LCR remains unknown. Questions that I am pursuing include the
structure/function relationships of the individual HSs composing the LCR, the structural
features that are required for formation of the LCR holocomplex, the mechanism of
interaction between the LCR and individual globin genes, and the mechanism whereby the LCR
activates chromosomal domains. In my studies, I utilize yeast artificial chromosomes
containing the entire beta-globin locus (beta-YACs). Mutations are introduced into the
beta-YACs by homologous recombination in yeast without leaving exogenous DNA; the YACs are
purified and microinjected into murine oocytes for the production of transgenic mice or
transfected into established cell lines. Thus, the effect of these mutations on LCR
function may be analyzed in the context of the intact beta-globin locus throughout
development. I also study other genetic regulatory mechanisms and disease pathogenesis
using transgenic mouse models of sickle cell disease, Alzheimer's disease, Kennedy's
disease, polycystic kidney disease and Alport's syndrome.
