Mary M. Weber, PhD

Assistant Professor of Microbiology and Immunology

Contact Information

Office: 3-370 Bowen Science Building
51 Newton Rd
Iowa City, IA 52242

Lab: 3-315M Bowen Science Building
51 Newton Rd
Iowa City, IA 52242


BS, Biology, University of Akron
MS, Biology, Texas State University
PhD, Biomedical Sciences, Texas A&M Health Science Center

Postdoctoral Fellow, Rocky Mountain Laboratories-NIH/NIAID

Education/Training Program Affiliations

Biomedical Science Program

Research Summary

My laboratory studies how obligate intracellular pathogens, such as chlamydia, subvert host defense mechanisms to establish their unique intracellular niche. Chlamydiae are obligate intracellular pathogens and a significant cause of morbidity in both humans and animals. C. trachomatis is the leading cause of preventable blindness worldwide and is the most commonly reported sexually transmitted infection worldwide. There is no effective vaccine and 3 million new cases are reported annually in the United States. Treatment, diagnosis, and prevention of chlamydial infections places a substantial strain on the healthcare industry each year, necessitating improved methods to treat and prevent disease.

All chlamydiae replicate in a membrane-bound compartment termed the inclusion. Early in the infection cycle, the pathogen modifies this compartment through the incorporation of specialized type III secreted proteins, referred to as inclusion membrane proteins (Incs). Incs are inserted into the inclusion membrane in such a way that their N- and C- termini are exposed to the host cytoplasm, perfectly positioning them at the host-pathogen interface. Using genetic, cellular, and molecular approaches, we have shown that a subset of Incs are required for in vitro and in vivo infection. The absence of specific Incs triggers premature inclusion lysis, truncation of the bacterial developmental cycle, activation of STING and autophagy pathways; culminating in premature host cell death. Building on these findings, our laboratory is currently interested in 1.) Elucidating the effector mechanism of specific inclusion membrane proteins 2.) Determining how chlamydiae modulate host cell death pathways and 3.) Determining if Incs play a role in serovar-specific disease. A better understanding of how chlamydia interacts with the host will provide much needed insight to develop new strategies for combatting this pathogen.


Weber, M. M., Lam, J. L., Dooley, C. A., Noriea, N. F., Hansen, B. T., Hoyt, F. H., Carmody, A. B., Sturdevant, G. L. & Hackstadt, T. (2017). Absence of Specific Chlamydia trachomatis Inclusion Membrane Proteins Triggers Premature Inclusion Membrane Lysis and Host Cell Death. Cell Rep, 19(7), 1406-1417. PMID: 28514660.

Wesolowski, J., Weber, M. M., Nawrotek, A., Dooley, C. A., Calderon, M., St Croix, C. M., Hackstadt, T., Cherfils, J. & Paumet, F. (2017). Chlamydia Hijacks ARF GTPases To Coordinate Microtubule Posttranslational Modifications and Golgi Complex Positioning. MBio, 8(3), e02280-16. PMID: 28465429.

Weber, M. M., Noriea, N. F., Bauler, L. D., Lam, J., Sager, J., Wesolowski, J., Paumet, F. & Hackstadt, T. (2016). A Functional Core of IncA Is Required for Chlamydia trachomatis Inclusion Fusion. J Bacteriol, 198(8), 1347-55. PMID: 26883826.

Weber, M. M., Faris, R., Tellez, A., Wright, W. U., Galvan, G., Luo, Z. Q. & Samuel, J. E. (2016). Modulation of the host transcriptome by Coxiella burnetii nuclear effector Cbu1314. Microbes Infect, 18(5), 336-45. PMID: 26827929.

Faris, R., Weber, M. M., Seeger, D. R., Cavazos, D., de Graffenried, L., Murphy, E. J. & Jolly, C. A. (2016). Mitochondrial Glycerol-3-Phosphate Acyltransferase-Dependent Phospholipid Synthesis Modulates Phospholipid Mass and IL-2 Production in Jurkat T Cells. Lipids, 51(3), 291-301. PMID: 26797755.

Weber, M. M., Faris, R., van Schaik, E. J., McLachlan, J. T., Wright, W. U., Tellez, A., Roman, V. A., Rowin, K., Case, E. D., Luo, Z. Q. & Samuel, J. E. (2016). The Type IV Secretion System Effector Protein CirA Stimulates the GTPase Activity of RhoA and Is Required for Virulence in a Mouse Model of Coxiella burnetii Infection. Infect Immun, 84(9), 2524-33. PMID: 27324482.

Weber, M. M., Bauler, L. D., Lam, J. & Hackstadt, T. (2015). Expression and localization of predicted inclusion membrane proteins in Chlamydia trachomatis. Infect Immun, 83(12), 4710-8. PMID: 26416906.

Weber, M. M., Chen, C., Rowin, K., Mertens, K., Galvan, G., Zhi, H., Dealing, C. M., Roman, V. A., Banga, S., Tan, Y., Luo, Z. Q. & Samuel, J. E. (2013). Identification of Coxiella burnetii type IV secretion substrates required for intracellular replication and Coxiella-containing vacuole formation. J Bacteriol, 195(17), 3914-24. PMID: 23813730.

van Schaik, E. J., Chen, C., Mertens, K., Weber, M. M. & Samuel, J. E. (2013). Molecular pathogenesis of the obligate intracellular bacterium Coxiella burnetii. Nat Rev Microbiol, 11(8), 561-73. PMID: 23797173.

Chu, W., Zere, T. R., Weber, M. M., Wood, T. K., Whiteley, M., Hidalgo-Romano, B., Valenzuela Jr, E. & McLean, R. J. (2012). Indole production promotes Escherichia coli mixed-culture growth with Pseudomonas aeruginosa by inhibiting quorum signaling. Appl Environ Microbiol, 78(2), 411-9. PMID: 22101045.

Weber, M. M., French, C. L., Barnes, M. B., Siegele, D. A. & McLean, R. J. (2010). A previously uncharacterized gene, yjfO (bsmA), influences Escherichia coli biofilm formation and stress response. Microbiology, 156(Pt 1), 139-47. PMID: 19833773.

Dusane, D. H., Zinjarde, S. S., Venugopalan, V. P., McLean, R. J., Weber, M. M. & Rahman, P. K. (2010). Quorum sensing: implications on rhamnolipid biosurfactant production. Biotechnol Genet Eng Rev, 27, 159-84. PMID: 21415897.

Chen, C., Banga, S., Mertens, K., Weber, M. M., Gorbaslieva, I., Tan, Y., Luo, Z. Q. & Samuel, J. E. (2010). Large-scale identification and translocation of type IV secretion substrates by Coxiella burnetii. Proc Natl Acad Sci U S A, 107(50), 21755-60. PMID: 21098666.