Christopher Burtner

Chris Burtner

Department: Biochemistry
Year Entered: 2005
Prior Degrees: BA, University of Puget Sound, 1999

Research Interests:
Advancements in medical care contribute to an increase in human life expectancy. As a result, it is predicted that by the year 2030 adults 65 years and older will account for one-fifth of the US population. These medical advancements have also brought about a shift in the leading causes of mortality from infectious diseases and acute illness to chronic diseases and degenerative illness. As a result of our longer average life span, medical care focuses on the treatment of age-associated disease. My research interests are broadly focused on understanding the biology behind the physiologic decline our bodies, tissues, and cells experience as we age.

I use two approaches for studying the basic biology of aging. In one approach, yeast is used to understand the changes that occur in single cells as a function of age. Yeast is amenable to genetic modification, and we take advantage of this to explore how aging may be regulated at the level of the genes. We have identified several genes whose deletion results in increased yeast life span, and we place these genes into genetic pathways to better understand aging in higher organisms.

In the second approach, it is useful to examine instances where the natural aging process goes awry, using information from human progerias and tissues that age prematurely. Hutchinson Gilford progeria syndrome (HGPS) is an exceedingly rare disorder that causes symptoms of advanced aging in certain tissues of the body. HGPS individuals display characteristics of advanced aging as children, including alopecia, loss of subcutaneous fat, osteolysis, and arterial disease. Myocardial infarction or stroke is often the cause of mortality in HGPS individuals, with a mean life span of 13.4 years. The molecular basis for the disease was identified in 2003 as a point mutation in the gene encoding A-type lamins, which are intermendiate filaments that localize to the nucleoplasmic side of nuclear envelope. To understand how a mutation in lamin A causes premature aging, we are investigating protein-protein interactions that are mediated by the nuclear lamina to identify the downstream molecular events that lead to the disease phenotype.

Participation in the Molecular Medicine program at the University of Washington has been a very rewarding training experience. It has provided me with the conceptual framework and vocabulary to allow me to evaluate the clinical significance of my basic research. My long term goal is to continue my research in the molecular and genetic causes of aging in order to develop therapies that may be useful in the treatment of age-associated disease.

Publications:
Burtner, C.R., Murakami, C.J., and Kaeberlein, M. (2009). A genomic approach to yeast chronological aging. Methods Mol Biol 548, 101-114.

Burtner, C.R., Murakami, C.J., Kennedy, B.K., and Kaeberlein, M. (2009). A molecular mechanism of chronological aging in yeast. Cell Cycle 8, 1256-1270.

Kudlow, B.A., Stanfel, M.N., Burtner, C.R., Johnston, E.D., and Kennedy, B.K. (2008). Suppression of proliferative defects associated with processing-defective lamin A mutants by hTERT or inactivation of p53. Mol Biol Cell 19, 5238-5248.

Murakami, C.J., Burtner, C.R., Kennedy, B.K., and Kaeberlein, M. (2008). A method for high-throughput quantitative analysis of yeast chronological life span. J Gerontol A Biol Sci Med Sci 63, 113-121.

Kaeberlein, M., Burtner, C.R., and Kennedy, B.K. (2007). Recent developments in yeast aging. PLoS Genet 3, e84.

Till, B.J., Reynolds, S.H., Weil, C., Springer, N., Burtner, C., Young, K., Bowers, E., Codomo, C.A., Enns, L.C., Odden, A.R., et al. (2004b). Discovery of induced point mutations in maize genes by TILLING. BMC Plant Biol 4, 12.

Till, B.J., Burtner, C., Comai, L., and Henikoff, S. (2004a). Mismatch cleavage by single-strand specific nucleases. Nucleic Acids Res 32, 2632-2641.

Comai, L., Young, K., Till, B.J., Reynolds, S.H., Greene, E.A., Codomo, C.A., Enns, L.C., Johnson, J.E., Burtner, C., Odden, A.R., et al. (2004). Efficient discovery of DNA polymorphisms in natural populations by Ecotilling. Plant J 37, 778-786.

Greene, E.A., Codomo, C.A., Taylor, N.E., Henikoff, J.G., Till, B.J., Reynolds, S.H., Enns, L.C., Burtner, C., Johnson, J.E., Odden, A.R., et al. (2003). Spectrum of chemically induced mutations from a large-scale reverse-genetic screen in Arabidopsis. Genetics 164, 731-740.

Till, B.J., Reynolds, S.H., Greene, E.A., Codomo, C.A., Enns, L.C., Johnson, J.E., Burtner, C., Odden, A.R., Young, K., Taylor, N.E., et al. (2003). Large-scale discovery of induced point mutations with high-throughput TILLING. Genome Res 13, 524-530.