jbeetham@iastate.edu
Homepage through the College of Veterinary Medicine.
Education
1994 Ph.D. Biochemistry and Biophysics, University of California at Davis
1989 B.S. Molecular and Cellular Biology, Western Washington University (minor Chemistry)
Research Experience
Postdoctoral Research Associate, University of Iowa, Department of Biochemistry (with John E. Donelson: gene regulation in Leishmania chagasi).
Postdoctoral Research Associate, University of California at Davis, Department of Entomology
Visiting Scientist, University of Mainz (Germany), Institute of Toxicology
Research Scientist, Western Washington University, Institute of Toxicology
Present Research: Dr. Beetham's research on protozoan parasites focuses on regulation of pathogenesis and the characterization of host-parasite-vector interactions, emphasizing Leishmania chagasi as a model system. Leishmania spp. are protozoan parasites that infect mammals and other vertebrates causing a collection of diseases that vary in severity from the self-healing to the potentially fatal. One goal of present research is to understand how Leishmania survive the innate immune response of mammals. Related studies have sought to identify and characterize genes and proteins that function to confer parasite resistance to serum lysis. A number of candidate genes/proteins have now been identified that may function in parasite resistance to serum lysis. Among these candidates is GP46, a predominant Leishmania surface glycoprotein that is normally upregulated only on serum-sensitive parasites and which we have shown confers serum resistance when expressed on serum-sensitive parasites. Ongoing studies seek a mechanistic understanding of GP46 function in serum resistance. A second goal of present research work is to determine mechanisms by which Leishmania regulate gene and protein expression during development and acquisition of pathogenesis. Leishmania spp. are unusual among eukaryotes in their almost complete reliance on post-transcriptional processes to regulate type-II gene expression; gene regulation at transcription is extremely rare. Furthermore, RNA processing in Leishmania is quite different from that which occurs in most eukaryotes, and molecules that function in RNA processing events (including those events that affect RNA stability) are therefore likely to be very different from the analogous factors of other eukaryotes. Understanding the mechanism by which Leishmania modulate the mRNA abundance of developmentally regulated genes/proteins, or by which the parasites survive innate host immune responses, may identify candidate molecular targets for new disease treatment modalities.
Selected Publications:
Lincoln, L.M., Ozaki, M., Donelson, J.E., and Beetham, J.K. (2004) Genetic complementation of Leishmania deficient in PSA (GP46) restores their resistance to lysis by complement. Molecular and Biochemical Parasitology 137, 185-189.
Beetham, J.K., Donelson, J.E. & Dahlin, R.R. (2003) Surface glycoprotein PSA (GP46) expression during short- and long-term culture of Leishmania chagasi. Mol Biochem Parasitol 131-2, 109-117.
Myung, K.S., Beetham, J.K., Wilson, M.E. & Donelson, J.E. (2002) Comparison of the post-transcriptional regulation of the mRNAs for the surface proteins PSA (GP46) and MSP (GP63) of Leishmania chagasi. J Biol Chem 277, 16489-97.
Morisseau, C., Beetham J.K., Pinot, F., Debernard, S., Newman, J.W. & Hammock, B.D. (2000). Cress and potato soluble epoxide hydrolases: purification, biochemical characterization, and comparison to mammalian enzymes. Arch Biochem Biophys 378(2): 321-32.
McCoy, J.J., Beetham, J.K., Ochs, D.E., Donelson, J.D., Wilson, M.E. (1998). Regulatory sequences and a novel gene in the msp (GP63) gene cluster of Leishmania chagasi. Mol. Biochem. Parasitol. 95:251-65.
Beetham, J.K., Myung, K.S., McCoy, J.J., Wilson, M.E., and Donelson, J.D. (1997). Glycoprotein 46 mRNA abundance is post-transcriptionally regulated during development of Leishmania chagasi promastigotes to an infectious form. J. Biol. Chem. 272, 17360-17366.