David Raskin, Ph.D.

Associate Professor of Microbiology 

David Raskin, Ph.D.


David Raskin, Ph.D. is an associate professor of microbiology at the Marian University College of Osteopathic Medicine. Dr. Raskin earned his B.S. in biology from The Ohio State University and M.S. in biology from the University of Dayton. He received his Ph.D. in molecular biology and microbiology from Case Western Reserve University. He performed a post-doctoral fellowship focusing on bacterial pathogenesis at Harvard Medical School. 

During his fellowship, Dr Raskin taught in the Immunology, Microbiology, and Infectious Disease course. After finishing his fellowship, he had a research laboratory at The Methodist Hospital Research Institute in Houston, Texas.

Dr. Raskin’s research interests are in bacterial genetics, physiology, and pathogenesis. In particular, he is interested in the regulation of virulence factors in the bacterium Vibrio cholerae, the causative agent of cholera.

Clinical/research interests

I am interested in bacterial pathogenesis. I focus on Vibrio cholerae, the causative agent of the epidemic diarrheal disease cholera. My laboratory uses genetics, biochemistry, cell biology and genomics to study how bacteria ‘sense’ their environment and use that information to regulate genes involved in virulence. V. cholerae is a normal component of aquatic environments, and when ingested, certain strains are able to exploit the human host and grow and reproduce rapidly in the small intestine. In the host, V. cholerae produce diarrheal symptoms that allow the bacteria to escape to the environment or to a new host. A number of virulence factors are necessary in order to produce cholera disease. In aquatic environments, V. cholerae form biofilms, which protect the bacteria from predation and also protect them from stomach acid when ingested. TCP, the toxin-coregulated pilus, is necessary in order to colonize the small intestine. Cholera toxin is a secreted toxin produced when the bacteria is in the small intestine that is primarily responsible for producing diarrhea. Biofilms are produced in the environment and not in the host, while cholera toxin and TCP are produced in the host, but not in aquatic environments.

I am interested in how V. cholerae determines whether it is in a host or an aquatic environment, and how it translates this information in order to regulate the genes responsible for these virulence factors. I am interested in identifying the particular environmental signals responsible for gene regulation in the environment and in the host and how this information is used to regulate the genes responsible for production of biofilm, TCP and cholera toxin. One particular signaling pathway that I am studying is the stringent response, a low nutrient stress response that is present in almost all free-living bacteria. Different environments have different nutrient levels, and I am characterizing how nutrient levels affect virulence factor expression through the stringent response.


Oh, Y.T., Lee, K.-M., Bari, W., Raskin, D.M., Yoon, S.S. 2015. A small nucleotide regulator, (p)ppGpp, directs the metabolic fate of glucose in Vibrio cholerae. J. Biol. Chem. 290:13178-13190.

Oh, Y.T., Park, Y., Yoon, M.Y., Bari, W., Go, J., Raskin, D.M., Lee, K.-M., Yoon, S.S. 2014. Cholera toxin production during anaerobic Trimethylamine N-oxide respiration is mediated by stringent response in Vibrio choleraeJ. Biol. Chem. 289:13232-13242.

He, H., Cooper, J.N., Mishra, A. and Raskin, D.M. 2012. Stringent response regulation of biofilm formation in Vibrio cholerae. J. Bacteriol. 194:2962-2972. 

Raskin, D.M., Judson, N., and Mekalanos, J.J. 2007. Regulation of the stringent response is the essential function of the conserved bacterial G protein CgtA in Vibrio cholerae. Proc. Natl. Acad. Sci. USA 104:4636-4641.

Raskin, D.M., Seshadri, R., Pukatzki, S.U., and Mekalanos, J.J. 2006. Bacterial genomics and pathogen evolution. Cell 124:703-714.

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