Christina L. Stallings, PhD

Molecular Microbiology

Molecular Microbiology and Microbial Pathogenesis Program
Immunology Program
Plant and Microbial Biosciences Program
Biochemistry, Biophysics, and Structural Biology Program

  • 314-286-0276

  • 314-286-0277

  • 314-362-3203

  • BJCIH 10303



  • bacteria, gene regulation, molecular genetics, microbiology, pathogenesis, transcription, infectious disease, innate immunity

  • Molecular pathogenesis of Mycobacterium tuberculosis

Research Abstract:

Research in the Stallings Laboratory seeks to better understand the incredible ability of Mycobacterium tuberculosis to withstand hostile conditions during infection and persist for the lifetime of the host.

M. tuberculosis infection begins when inhaled bacilli enter the airways and are immediately exposed to phagocytic cells of the innate immune system. Infection of naive alveolar macrophages and dendritic cells leads to a proinflammatory response and the recruitment of lymphocytes, monocytes, and fibroblasts to form a granuloma. Within the granuloma, the infected cells are activated to kill the intracellular bacteria by imposing an arsenal of stresses. Despite this onslaught of stresses, the bacteria are able to persist for the lifetime of the host, indicating that M. tuberculosis mounts a significant defense against the immune system.

We have identified a number of mycobacterial proteins that function as mediators of mycobacterial stress responses and are required for pathogenesis. Our lab continues to investigate the roles of these proteins during infection and how their activities can be inhibited in new chemotherapeutic strategies to treat mycobacterial infections. In addition, we are investigating the host responses necessary to control M. tuberculosis infection and prevent active tuberculosis disease.

Selected Publications:

Huynh, J.P., Lin, C., Kimmey, J.M., Jarjour, N.N., Schwarzkopf, E.A., Bradstreet, T.R., Shchukina, I., Shpynov, O., Weaver, C.T., Taneja, R., Artyomov, M.N., Edelson, B.T., and Stallings, C.L.. 2018. Bhlhe40 is an essential repressor of IL-10 during Mycobacterium tuberculosis infection. The Journal of Experimental Medicine. In Press. PMID: 29773644.

Prusa, J., Jensen, D., Santiago-Collazo, G., Pope, S.S., Garner, A.L., Miller, J.J., Ruiz Manzano, A., Galburt, E.A., and Stallings, C.L.. 2018. Domains within RbpA serve specific functional roles that regulate distinct mycobacterial gene subsets. Journal of Bacteriology. In Press. PMID: 29686140.

Nair, S., Huynh, J.P., Lampropoulou, V., Loginicheva, E., Esaulova, E., Gounder, A.P., Boon, A.C.M., Schwarzkopf, E.A., Bradstreet, T.R,. Edelson, B.T., Artyomov, M.N., Stallings, C.L.*, and Diamond, M.S.*. 2018. Irg1 expression in myeloid cells prevents immunopathology during Mycobacterium tuberculosis infection. The Journal of Experimental Medicine. 215(4):1035-1045. PMCID: PMC5881474. (*Co-corresponding authors)

Mann, K.M., Huang, D.L., Hooppaw A.J., Logsdon, M.M., Richardson, K., Lee, H.J., Kimmey, J.M., Aldridge, B.B., and Stallings, C.L.. 2017. Rv0004 is a new essential member of the mycobacterial DNA replication machinery. PLOS Genetics. 13(11):e1007115. PMID: 29176877.

Kimmey, J.M., Huynh, J.P., Weiss, L.A., Park, S., Kambal, A., Debnath, J., Virgin, H.W., and Stallings, C.L.. 2015. Unique role for ATG5 in neutrophil-mediated immunopathology during M. tuberculosis infection. Nature. 528(7583):565-9. PMCID: PMC4842313.

Garner, A.L., Weiss, L.A., Ruiz Manzano, A., Galburt, E.A., and Stallings, C.L.. 2014. CarD integrates three functional modules to promote efficient transcription, antibiotic tolerance, and pathogenesis in mycobacteria. Molecular Microbiology. 93(4):682-97. PMCID: PMC4127138.

Weiss, L.A. and Stallings, C.L.. 2013. Essential Roles for Mycobacterium tuberculosis RelMtb beyond the production of (p)ppGpp. Under revision for JBac.

Srivastava, D. B., Leon, K, Osmundson, J, Garner, A., Weiss, L. A., Westblade, L., Glickman, M. S., Landick, R., Darst, S. A., and *Stallings, C. L., and *Campbell, E.A.. 2013. Structure and function of CarD, an essential Mycobacterial transcription factor. PNAS. 110(31):12619-24. PMID: 23858468. (*Co-corresponding authors).

Roxane Tussiwand, Wan-Ling Lee, Theresa L. Murphy, Mona Mashayekhi, Jrn C. Albring, Ansuman T. Satpathy, Wumesh KC, Jeffrey A. Rotondo, Brian T. Edelson, Nicole M. Kretzer, Xiaodi Wu, Michael Behnke, Leslie A. Weiss, Samuel S.K. Lam, Cora T. Aurthur, Christina L. Stallings, L. David Sibley, Robert D. Schreiber, and Kenneth M. Murphy. 2012. BATF leucine zipper-dependent interactions with IRF factors mediate class switch recombination, TH17 development and a novel Batf3-independent pathway of CD8a+ cDC development. Nature. 490(7421):502-7. PMID: 22992524.

Weiss, L. A., Harrison, P. G., Nickels, B. E., Glickman, M. S., Campbell, E. A., Darst, S. A., and Stallings, C. L. 2012. The interaction of CarD with RNAP mediates Mycobacterium tuberculosis viability, rifampicin resistance, and persistence. JBac. 194(20):5621-31. PMID: 22904282.

Last Updated: 11/7/2022 1:38:13 PM

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