Jon T. Skare, Ph.D.

Jon T. Skare, Ph.D.

Professor and Associate Chair

Department of Microbial Pathogenesis and Immunology
8447 State Highway 47, MREB #3004
Bryan, TX   77807

Phone: 979-436-0353
Fax: 979-436-0360

Education and Post-Graduate Training

B.S. University of California at Irvine (1986)

Ph.D. Washington State University (1992)

Postdoc. University of California-Los Angeles (1992-96)

Research Interests

My laboratory studies Borrelia burgdorferi, the spirochetal bacterium that causes Lyme disease. B. burgdorferi is the most common arthropod-borne infectious agent in the United States, with over 35,000 cases reported to the CDC in 2008. This number represented a 30% increase from the previous year, indicating that B. burgdorferi is a re-emerging infectious agent.

The goals of my research are to understand how B. burgdorferi causes disease and adapts to different niches it occupies by: (1) addressing the role of attachment, colonization and subsequent dissemination using newly developed genetic methodologies to inactivate genes involved in adherence of B. burgdorferi to host tissues; and (2) understanding how B. burgdorferi responds to oxidative stress via the function of the global regulatory protein BosR.

In regard to the first project, and in collaboration with Magnus Höök’s group, we are studying how binding by B. burgdorferi to host structures impacts the infectious process.  Our initial studies evaluated the role of the fibronectin binding protein of B. burgdorferi (BBK32) in borrelial pathogenesis. This work suggested that BBK32 is required for full virulence in the mouse animal model system of Lyme borreliosis.  Subsequent studies have focused on the borrelial decorin binding protein adhesins, DbpBA.  When the dbpBA genes are deleted from B. burgdorferi, the spirochetes are significantly attenuated in the mouse model of infection, indicating that the Dbp proteins are essential for maximum virulence of B. burgdorferi.  We are currently addressing how additional B. burgdorferi proteins affect colonization, dissemination, and persistence, as well as how they alter the host immune response, to further elucidate the importance of these borrelial proteins in Lyme pathogenesis.

For the second project, the role of the BosR oxidative stress regulator is being addressed. The BosR protein is a homologue to the PerR regulator, a protein whose activity in other bacterial systems is associated with a response to oxidative stressors.  Using both biochemical and genomic based approaches, we have identified several genes, including the lone superoxide dismutase encoded by B. burgdorferi, that are putatively regulated by BosR.  We contend that B. burgdorferi responds to the redox status of its locale and uses this, in addition to pH and temperature, as a cue to modulate gene expression in order to adapt to its environment via BosR as well as other regulatory pathways.  Along these lines, we have recently found that BosR interfaces with the Rrp2-RpoN-RpoS regulatory cascade to alter the expression of genes and the production of proteins involved in borrelial pathogenesis.  As such, BosR is critical for both physiological and pathogenic properties of B. burgdorferi.

Research Laboratory Members

Post Doc

Graduate Students

  • Hui Zhi
  • Diana Medina


  • Katherine Biancardi
  • Caleb Grimes
  • Lauren Weise

Selected Publications

Shaw, D. K., Hyde, J. A., and J. T. Skare. 2012.  The BB0646 protein demonstrates lipase and hemolytic activity associated with Borrelia burgdorferi, the etiological agent of Lyme disease. Mol Microbiol. 83(2):319-334.

Hyde, J.A., Weening, E.H., Chang, M.H., Trzeciakowski, J.P., Höök, M., Cirillo, J.D., and J. T. Skare.  2011.  Bioluminescent imaging of Borrelia burgdorferi in vivo demonstrates that the fibronectin binding protein BBK32 is required for optimal infectivity. Mol Microbiol. 82(1): 99-113.

Wu, J., Weening, E. H., Faske, J., Höök, M. and J. T. Skare. 2011. Invasion of eukaryotic cells by Borrelia burgdorferi requires β₁ integrins and Src kinase activity. Infect Immun., 79(3): 1338-1348.

Hyde, J.A., Weening, E.H., and J. T. Skare.  2011. Genetic Transformation of Borrelia burgdorferi. Curr Protoc Microbiol. Unit 12C.4.1-17.

Gherardini, F.C., Boylan, J., Lawrence, K. and J.T. Skare. 2010.  Metabolism and Physiology of Borrelia.  In Borrelia: Molecular and Cellular Biology.  Samuels, D.S. and Radolf, J.D. (eds).  Norfolk: Caister Academic Press: 103-138.

Skare, J.T., Carroll J.A., Yang, X.F., Samuels, D.S. and D.R. Akins. 2010.  Gene Regulation, Transcriptomics, and Proteomics.  In Borrelia: Molecular and Cellular Biology.  Samuels, D.S. and Radolf, J.D. (eds).  Norfolk: Caister Academic Press: 67-101

Hyde, J.A., Shaw, D.K., Smith, R., Trzeciakowski, J.P., and J. T. Skare.  2010. Characterization of a Conditional bosR Mutant in Borrelia burgdorferi. Infect. Immun. 78(1): 265-274.

Hyde, J.A., Shaw, D.K., Smith, R., Trzeciakowski, J.P., and J. T. Skare.  2009.  The BosR regulatory protein of Borrelia burgdorferi interfaces with the RpoS regulatory pathway and modulates both the oxidative stress response and pathogenic properties of the Lyme disease spirochete. Mol Microbiol. 74(6): 1344-1355.

Prabhakaran, S., Liang, X., Skare, J. T., Potts, J. R. and M. Höök.  2009.  A Novel Fibronectin Binding Motif in MSCRAMMs Targets F3 Modules.  PLoS ONE 4(4): e5412.

Weening E. H., Parveen. N., Trzeciakowski, J. P., Leong, J. M., Höök, M., and J. T.  Skare.  2008. Borrelia burgdorferi Lacking DbpBA Exhibit an Early Survival Defect During Experimental Infection. Infect. Immun. 76(12): 5694-5705.

Hyde, J. A., Trzeciakowski, J. P. and J. T. Skare. 2007. Borrelia burgdorferi alters its gene expression and antigenic profile in response to CO2 levels. J. Bacteriol. 189(2): 437-445.

Hyde, J. A., Seshu, J. and J. T. Skare. 2006. Transcriptional Profiling of Borrelia burgdorferi Containing a Unique bosR Allele Identifies a Putative Oxidative Stress Regulon. Microbiology 152(9): 2599-2609.

Seshu, J., M. Labandeira-Rey, M. D. Esteve-Gassent, M. Höök, and J. T. Skare. 2006. The Isolation and Characterization of Isogenic Mutants in Infectious Borrelia burgdorferi. NATO Meeting Proceedings, Advanced Research Workshop, IOS Press., F. C. Cabello et al. (Eds.), pp. 25-41.

Seshu, J., Esteve-Gassent, M. D., Labandeira-Rey, M., Kim, J. H., Trzeciakowski, J. P., Höök, M. and J. T. Skare. 2006. Inactivation of the Fibronectin Adhesin Gene bbk32 Significantly Attenuates the Infectivity Potential of Borrelia burgdorferi. Mol Microbiol. 59(5): 1591-1601.

Seshu, J., Boylan, J. A., Hyde, J. A., Swingle, K. L., Gherardini, F. C. and J. T. Skare. 2004. A Conservative Amino Acid Change Alters the Regulatory Activity of BosR, the Redox Regulator of Borrelia burgdorferi. Mol. Microbiol. 54(5): 1352-1363.

Seshu, J., Boylan, J., Gherardini, F. C. and J. T. Skare. 2004. Dissolved Oxygen Levels Alter Gene Expression and Antigen Profiles in Borrelia burgdorferi. Infect Immun . 72(3): 1580-1586.

Labandeira-Rey, M. Seshu J., and J. T. Skare. 2003. The Absence of Linear Plasmid 25 (lp25) or 28-1 (lp28-1) of Borrelia burgdorferi Dramatically Alters the Kinetics of Experimental Infection Via Distinct Mechanisms. Infect Immun . 71(8): 4608-4613.

Ojaimi, C., Brooks, C., Casjens, S., Rosa, P., Elias, A., Barbour, A., Jasinskas, A., Benach, J., Katona, L., Radolf, J., Caimano, M., Skare, J., Swingle, K., Akins, D., and I. Schwartz. 2003. Profiling Temperature-induced Changes in Borrelia burgdorferi Gene Expression using Whole Genome Arrays. Infect. Immun . 71(4): 1689-1705.

Ojaimi, C., Brooks, C., Akins, D., Casjens, S., Rosa, P., Elias, A., Barbour, A., Jasinskas, A., Benach, J., Katona, L., Radolf, J., Caimano, M., Skare, J., Swingle, K., Sims, S. and I. Schwartz. 2002. Borrelia burgdorferi Gene Expression Profiling with Membrane-Based Arrays. Methods Enzymol . 358: 165-177 .

McDowell, J.V., Sung, S. Y., Labandeira-Rey, M., Skare, J. T., and R. T. Marconi. 2001. Analysis of Mechanisms Associated with the Loss of Infectivity of Clonal Populations of Borrelia burgdorferi B31 MI. Infect. Immun . 69(6): 3670-3677.

Labandeira-Rey, M. and J. T. Skare. 2001. Decreased Infectivity in Borrelia burgdorferi strain B31 is Associated with the Loss of Either Linear Plasmid 25 or 28-1. Infect. Immun. 69(1): 446-455