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Guangchun Bai , Ph.D. , M.D.
Assistant Professor


1991 - M.D. from Fourth Military Medical University, China
1999 - Ph.D. from Fourth Military Medical University, China

Current Research

Our work focuses on bacterial gene regulation and pathogenesis. Currently we are interested in two pathogens, Mycobacterium tuberculosis and Streptococcus pneumoniae. The long-term objective of this laboratory is to better understand the molecular basis of these pathogens for establishing effective strategies of prevention and therapy. We generally employ multiple approaches including genetics, biochemistry, molecular biology and cellular biology to study these pathogens.


M. tuberculosis is the causative agent of tuberculosis, which has successfully infected about one-third of the world’s population. Although an attenuated vaccine, M. bovis BCG, was available almost a century ago and anti-tubercular drugs have been exploited for many decades, the current strategies are still inadequate to control the prevalence. For this pathogen, our primary interest focuses on how cyclic nucleotides, especially c-di-AMP and c-di-GMP, contribute to the bacterial pathogenesis at molecular and cellular levels. Additionally, we are also interested in screening compounds as potential anti-TB drugs to specifically block the bacterial metabolism pathways. 


S. pneumoniae is a commensal of the human respiratory tract, but it can still cause a variety of infections, such as pneumonia, meningitis, otitis media and bacteremia. Although a plethora of virulence determinants have been recognized in this pathogen, it remains largely unknown about how metabolic pathways enable the pathogen to acquire nutrients and cause diseases. A recent genome-wide mutagenesis study mapped 169 pneumococcal genes that were essential in an otitis media model. These genes include two members in the bacterial arginine deiminase pathway, arcD and arcT. We are currently exploring the molecular mechanism of the attenuation by deletion of these arc genes.

PubMed Publications

  1. Bai Y, Yang J, Zhou X, Ding X, Eisele LE, Bai G. Mycobacterium tuberculosis Rv3586 (DacA) is a diadenylate cyclase that converts ATP or ADP into c-di-AMP. PLoS One. 2012;7(4):e35206

  2. El Qaidi S, Yang J, Zhang JR, Metzger DW, Bai G. The vitamin B6 biosynthesis pathway in Streptococcus pneumoniae is controlled by pyridoxal 5'-phosphate and the transcription factor PdxR and has an impact on ear infection. J Bacteriol. 2013 May;195(10):2187-96

  3. Gupta R, Yang J, Dong Y, Swiatlo E, Zhang JR, Metzger DW, Bai G. Deletion of arcD in Streptococcus pneumoniae D39 impairs its capsule and attenuates virulence. Infect Immun. 2013 Oct;81(10):3903-11

  4. Bai Y, Yang J, Eisele LE, Underwood AJ, Koestler BJ, Waters CM, Metzger DW, Bai G. Two DHH subfamily 1 proteins in Streptococcus pneumoniae possess cyclic di-AMP phosphodiesterase activity and affect bacterial growth and virulence. J Bacteriol. 2013 Nov;195(22):5123-32

  5. Bai Y, Yang J, Zarrella TM, Zhang Y, Metzger DW, Bai G. Cyclic di-AMP impairs potassium uptake mediated by a cyclic di-AMP binding protein in Streptococcus pneumoniae. J Bacteriol. 2014 Feb;196(3):614-23

  6. Yang J, Bai Y, Zhang Y, Gabrielle VD, Jin L, Bai G. Deletion of the cyclic di-AMP phosphodiesterase gene (cnpB) in Mycobacterium tuberculosis leads to reduced virulence in a mouse model of infection. Mol Microbiol. 2014 Jul;93(1):65-79

  7. Underwood AJ, Zhang Y, Metzger DW, Bai G. Detection of cyclic di-AMP using a competitive ELISA with a unique pneumococcal cyclic di-AMP binding protein. J Microbiol Methods. 2014 Dec;107:58-62