M.D., Johns Hopkins University, 1985
University of California, Irvine
B-228 Medical Sciences I
Irvine, CA 92697-1700
Office: (949) 824-3397
Lab: (949) 824-3396
mingt@uci.edu
UCI Faculty Profile
Gene expression, pathogenesis and treatment of the human pathogen, Chlamydia
Our research in the fields of bacterial pathogenesis and infectious diseases looks at how the intracellular bacterium, Chlamydia, causes disease. Chlamydial infections are the most commonly reported infectious disease in the country. Chlamydia trachomatis is the most common cause of bacterial sexually transmitted disease in the developed world, and a leading cause of preventable blindness in the developing world. A second species, Chlamydia pneumoniae, has been associated with atherosclerotic heart disease. All chlamydial species share an unusual developmental life cycle that takes place within a eukaryotic host cell. To understand this life cycle, and how chlamydiae survive and replicate inside mammalian cells to cause disease, we have been studying how the organism regulates the expression of its genes. Using molecular biology, biochemistry and bioinformatics approaches, we have been studying the components involved in transcriptional regulation of gene expression, including RNA polymerase, the promoter structure that polymerase recognizes, and cis-acting DNA elements and trans-acting factors that modulate promoter activity. In particular, we are interested in how transcription factors, such as activators and repressors, and alternative RNA polymerase can coordinately regulated subsets of genes in response to environmental and metabolic signals. We are also studying how DNA supercoiling can function on a global level to regulate gene expression both at the level of promoter activity and transcriptional regulation. In addition to these gene expression studies, we are examining the effect of antimicrobial peptides against chlamydiae as an approach to develop new antichlamydial antibiotics.
UCI Faculty Profile: Ming Tan.
Yu, H.H.Y., Kibler, D. and Tan, M. In silico prediction and functional validation of sigma28-regulated genes in Chlamydia and E. coli. J. Bacteriol. 188: 8206-8212, 2006.
Tan, M. Regulation of gene expression. In Chlamydia: Genomics and Pathogenesis, P. Bavoil and P. Wyrick, eds., (Horizon Scientific Press, Wymondham, U.K.), in press, 2006.
Yu, H.H.Y., Di Russo, E.G., Rounds, M.A. and Tan, M. Mutational analysis of the promoter recognized by Chlamydia and E. coli sigma 28 RNA polymerase. J. Bacteriol. 188: 5524-5531, 2006.
Akers, J.C. and Tan, M. Molecular mechanism of tryptophan-dependent transcriptional regulation in Chlamydia trachomatis. J. Bacteriol. 188: 4236-4243, 2006.
Schaumburg, C.S., and Tan, M. Arginine-dependent gene regulation via the ArgR repressor is species-specific in Chlamydia. J. Bacteriol. 188: 919-927, 2006.
Wilson, A.C., Christine C. Wu, John R. Yates, III, and Tan, M. Chlamydial GroEL auto-regulates its own expression through direct interactions with the HrcA repressor protein. J. Bacteriol. 187: 7535-7542, 2005.
Wilson, A.C., and Tan, M. Stress response gene regulation in Chlamydia is dependent on HrcA-CIRCE interactions. J. Bacteriol. 186: 3384-3391, 2004.
Yu, H.H.Y. and Tan, M. Sigma 28 RNA polymerase regulates hctB, a late developmental gene in Chlamydia. Molecular Microbiology 50: 577-584, 2003.
Schaumburg, C.S., and Tan, M. Mutational analysis of the Chlamydia trachomatis dnaK promoter defines the optimal -35 promoter element. Nucleic Acids Research 31:551-555, 2003.
Wilson, A.C., and Tan, M. Functional analysis of the heat shock regulator HrcA of Chlamydia trachomatis. J. Bacteriol. 184: 6566-6571, 2002.
List of Publications via PubMed (NIH National Library of Medicine)