Man-Wah Tan

Administrative Appointments

• Senator-at-Large, School of Medicine Faculty Senate (2006 - present)

Honors and Awards

• V Foundation Scholar, V Foundation (2002)
• Basil O'Connor Scholar, March of Dimes (2002)
• Baxter Foundation Scholar, Baxter Foundation (2001)
• Junior Fellow, Harvard Society of Fellows (1997)

Professional Education

Postdoctoral Advisees

Fanglian He

Graduate & Fellowship Program Affiliations

• Genetics
• Immunology
• Microbiology and Immunology

Community & International Work

• New biopharmaceuticals against infectious agents, Penang, Malaysia 
• Host responses to virulence factors from B. pseudomallei, Bangi, Malaysia 

Web Site Links

• Tan Lab Home Page

Research Interests

I am interested in addressing the fundamental questions of how two antagonistic biological systems interact. My system of choice is the interaction between pathogenic bacteria and their metazoan hosts. Pathogenic bacteria constitute a serious threat to global health and have evolved a variety of strategies to defeat their hosts. A critical first line of defense that is evolutionarily conserved across metazoans is the innate immune system. It enables the host to recognize the aggressors and to communicate this information between and within the cells to elicit appropriate responses to pathogens. Innate immunity involves multiplicity of signaling pathways and effector mechanisms that often function redundantly against a broad spectrum of microbial threats. These molecular factors and signaling cascades function cell autonomously within infected tissues or produce extracellular factors to elicit their effects non-cell autonomously on other tissues. For the elucidation of both cell and non-cell autonomous events, and to gain a more holistic understanding of host-pathogen interactions within the context of a whole organism, I pioneered the use of infection of the nematode C. elegans by bacterial pathogens as the experimental system (Tan and Ausubel, 2000). With this system, both C. elegans and pathogen can be genetically altered and the effects of these alterations on pathogenesis or host immunity can be readily tested. We can also tap into the multifaceted power of genetics and genomics to elucidate the molecular and cellular mechanisms underlying host pathogen interactions in vivo. Because the C. elegans body is transparent, we are able assess the effects of loss- or gain- of a host protein function on the progress of infection simply by visualizing and quantifying the accumulation of fluorescently-labeled bacteria within these animals over time. Spatiotemporal changes in host genes expressions and the subcellular localization host proteins can also be assessed over...

Publications

• Gamma-linolenic and stearidonic acids are required for basal immunity in Caenorhabditis elegans through their effects on p38 MAP kinase activity. Nandakumar M, Tan MW. PLoS Genet. 2008; 4 (11): e1000273
• Pseudomonas aeruginosa suppresses host immunity by activating the DAF-2 insulin-like signaling pathway in Caenorhabditis elegans. Evans EA, Kawli T, Tan MW. PLoS Pathog. 2008; 4 (10): e1000175
• Neuroendocrine signals modulate the innate immunity of Caenorhabditis elegans through insulin signaling Kawli T, Tan MW. Nat Immunol. 2008; 9 (12): 1415-24
• A conserved role for a GATA transcription factor in regulating epithelial innate immune responses. Shapira M, Hamlin BJ, Rong J, Chen K, Ronen M, Tan MW. Proc Natl Acad Sci U S A. 2006; 103 (38): 14086-91
• A conserved p38 MAP kinase pathway in Caenorhabditis elegans innate immunity. Kim DH, Feinbaum R, Alloing G, Emerson FE, Garsin DA, Inoue H, Tanaka-Hino M, Hisamoto N, Matsumoto K, Tan MW, Ausubel FM. Science. 2002; 297 (5581): 623-6