Ming Tan

Professor, Microbiology & Molecular Genetics
School of Medicine

Professor, Medicine
School of Medicine

B.S., University of Florida, 1981


M.D., Johns Hopkins University, 1985

Phone: (949) 824-3397
Fax: (949) 824-8598
Email: mingt@uci.edu

University of California, Irvine
B240 Med Sci
Mail Code: 4025
Irvine, CA 92697

picture of Ming  Tan

Research
Interests
Chlamydia, bacterial pathogenesis, gene regulation, gene expression, transcription, host-pathogen interactions, protease, centrosome, cancer, infectious disease, sexually transmitted, infertility, trachoma, blindness
   
URLs Department of Microbiology & Molecular Genetics webpage
   
Tan Lab webpage
   
Academic
Distinctions
Clinical Investigator Award (K08), NIH
Established Investigator Grant, American Heart Association
Independent Scientist Award (K02), NIH
Fellow, Infectious Diseases Society of America
Dean’s Junior Physician/Scientist Award, College of Medicine, UC Irvine
Excellence in Teaching Award, School of Medicine, UC Irvine: 2004-2016 (8 times)
   
Appointments To apply for a postdoctoral position in my research group, please email me, describing your research interests and goals and attaching your CV.
   
Research
Abstract
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. In addition, genital strains of C. trachomatis have been associated with cervical cancer. A second species, Chlamydia pneumoniae is a common cause of community-acquired pneumonia.

All chlamydial species share an unusual developmental life cycle that takes place within a eukaryotic host cell. We are studying a number of aspects of this intracellular infection:

1. Gene regulation: A central question is how this pathogen replicates and converts between two developmental forms within an infected host cell. We are currently studying mechanisms of temporal regulation that control the expression of chlamydial genes at early, mid and late time points in the infectious cycle. These mechanisms include transcription factors, such as activators and repressors, alternative forms of RNA polymerase, and DNA supercoiling as a global regulator of gene expression. The approaches used include molecular biology, biochemistry, genetic approaches and bioinformatics. We are also using 3D electron microscopy to study how chlamydiae use cell size to control developmental conversion.

2. Host-pathogen interactions: Chlamydia manipulates and subverts numerous host processes in order to support its intracellular infection. We are studying how Chlamydia causes centrosome dysregulation such as the production of multiple centrosomes. These studies may provide a potential mechanism to explain the epidemiologic association of C. trachomatis and cervical cancer. We are also studying how Chlamydia causes loss of primary cilia, which is a signaling organelle on the host cell, and disrupts motile cilia, which may lead to infertility in women. These Chlamydia cell biology studies are a collaboration with Dr. Christine Suetterlin of the Department of Developmental and Cell Biology. Together, we are using a variety of cell biology approaches including immunofluorescent and electron microscopy, and protein analysis.
   
Publications Cheng, E. and Tan, M. Differential effect of DNA supercoiling on Chlamydia early promoters correlates with expression pattern in midcycle. J. Bacteriol. 194: 3109-3115, 2012.

Rosario, C.J. and Tan, M. The early gene product EUO is a transcripitional repressor that selectively regulates promoters of Chlamydia late genes. Mol. Microbiol. 84:1097-1107, 2012.

Chen, A.L., Johnson, K.A., Lee, J.K., Sütterlin, C. and Tan, M. CPAF: A Chlamydial protease in search of an authentic substrate. PLoS Pathog. 8:e1002842, 2012. (Selected for Faculty of 1000)

Rosario, C.J., Hanson, B.R. and Tan, M. The transcriptional repressor EUO regulates both subsets of Chlamydia late genes. Mol. Microbiol. 2014. 94:888-897.

Tan, M. and Sütterlin, C. The Chlamydia protease CPAF: Caution, Precautions And Function. Pathog Dis. 2014. 72:7-9.

Johnson, K.A.*, Lee, J.K.*, Chen, A.L., Tan, M. and Sütterlin, C. Induction and inhibition of CPAF activity during analysis of Chlamydia-infected cells, Pathog Dis. 2015, 73:1-8.

Hanson, B.R. and Tan, M. Transcriptional regulation of the Chlamydia heat shock stress response in an intracellular infection. Mol. Microbiol. 2015. 97:1158-1167.

Hanson, B.R., Slepenkin, A., Peterson,, E.M. and Tan, M. Chlamydia trachomatis type III secretion proteins regulate transcription. J. Bacteriol. 2015. 197: 3238-3244.

Rosario, C.J. and Tan, M. Regulation of Chlamydia gene expression by tandem promoters with different temporal patterns. J. Bacteriol. 2015. 198: 363-369.

Orillard, E. and Tan, M. Functional analysis of three topoisomerases that regulate DNA supercoiling levels in Chlamydia. Mol. Microbiol. 2016. 99:484-496.

Hanson, B.R. and Tan, M. Intra-ChIP: studying gene regulation in an intracellular pathogen. Curr. Genet. 2016. 62:547-551.
   
  Books:
Tan, M. and Bavoil, P.M. (ed.). Intracellular Pathogens I: Chlamydiales (Tan, M., Lead Editor) (ASM Press, Washington, DC), 2012.

Palmer, G.H. and Azad, A. (ed.). Intracellular Pathogens II: Rickettsiales (Tan, M., Lead Editor) (ASM Press, Washington, DC), 2012.


Book chapters:
Tan, M. and Bavoil, P.M. Introduction: Current and Future Aspects of Chlamydia Research. In Intracellular Pathogens I: Chlamydia. M. Tan and P.M. Bavoil, ed., (ASM Press, Washington, DC), 2012.

Tan, M. Temporal gene regulation during the chlamydial development cycle. In Intracellular Pathogens I: Chlamydiales. M. Tan and P.M. Bavoil, ed., (ASM Press, Washington, DC), 2012.
   
Grants R01 AI044198, NIAID, NIH, 5/17-4/22, “Mechanisms of developmental regulation in Chlamydia”
   
R01 AI123998, NIAID, NIH, 8/17-7/21, “Late developmental regulation in Chlamydia”
   
R21 AI117463, NIAID, NIH, 2/16-1/18, “Three-dimensional analysis and modeling of the Chlamydia developmental cycle”
   
R21 AI128723, NIAID, NIH, 6/17-5/19, “Effects of Chlamydia infection on motile cilia”
   
Professional
Societies
American Society for Microbiology: Division D (Bacteria of Medical Importance) Chair (2005-6), Division Advisor (2006-7)
Chlamydia Basic Research Society: Secretary-Treasurer (2007-11), President-Elect (2011-2013), President (2013-2015)
Infectious Diseases Society of America: Fellow
   
Graduate Programs Cellular and Molecular Biosciences

Infectious Disease (IM)

   
Research Center UC Irvine Chao Family Comprehensive Cancer Center
   
   
Link to this profile http://www.faculty.uci.edu/profile.cfm?faculty_id=4507
   
Last updated 11/13/2017