Jon T. Skare, PhD

Regent's Professor

Associate Head

Contact

Microbial Pathogenesis & Immunology
8447 Riverside Pkwy
Medical Research & Education Building Room 3004,
Bryan, TX 77807
jskare@tamu.edu
Phone: 979.436.0353
Fax: 979.436.0360
Skare Lab

Education and Training

University of California at Irvine, BS, 1986
Washington State University, PhD, 1992
University of California-Los Angeles, Postdoc, 1996

Research Interests

The Skare is focused on microbial pathogenesis with an emphasis in spirochetal infections, particularly Borreliella burgdorferi, the etiologic agent of Lyme disease, as well as Borrelia spp. spirochetes associated with relapsing fever. The long-term interests of the Skare lab center on understanding how B. burgdorferi promotes its pathogenic potential and persists in the disparate hosts it occupies in nature (e.g., both arthropods and mammals). In this regard, research is aligned with:
(i) Regulatory pathways that contribute to the establishment of infection during the arthropod to mammalian transition
(ii) Characterizing the response to oxidative stressors in B. burgdorferi and the regulation thereof
(iii) Identifying and characterizing surface structures that contribute to the colonization and maintenance of infection via adherence mechanisms
(iv) Understanding the ability of B. burgdorferi to persistently infect hosts in the face of a potent innate and adaptive immune response.

Awards, Recognition and Service

2023 Regents Professor

Representative Publications

Garrigues, R.J., Powell, A.D., Hammel, M., Skare, J.T.†, and B.L. Garcia†. 2021. A structural basis for inhibition of the complement initiator protease C1r by Lyme disease spirochetes. J. Immunol. 207 (11): 2856-2867. Link
†indicates co-corresponding authors
Booth, C.E.¶, Powell-Pierce¶, A.D., Skare, J.T.†, and B.L. Garcia†. 2022. Borrelia miyamotoi FbpA and FbpB are immunomodulatory outer surface lipoproteins with distinct structures and functions. Front. Immunol. 13: e886733. Link
PMID: 35693799 ¶ indicates co-first author; †indicates co-corresponding authors
Barnes A., Khandelwal S., Sartoretto S., Myoung S., Francis S.J., Lee G.M., Rauova L., Cines D.B., Skare J.T., Booth C.J., Garcia B.L., and G.M. Arepally. 2022. Minimal role for the alternative pathway in complement activation by HIT immune complexes. J. Throm Haem. 20: 2656-2665. doi.10.1111/jth.15856. PMID: 35996342
Coburn, J., Garcia, B., Hu. L., M. Jewett, P. Kraiczy, S. Norris, and J. Skare. 2021. Lyme Disease Pathogenesis. Curr Issues Mol Biol. 42: 473-518. doi: 10.21775/cimb.042.473 PMID: 33353871.
G. Chaconas, Moriarty, T., Skare, J., and J. Hyde. 2021. Live Imaging of Borrelial Infections. Curr Issues Mol Biol. 42: 385-408. doi: 10.21775/cimb.042.385. PMID: 33310914.
Skare, J.T. and B.L. Garcia. 2020. Complement Evasion by Lyme Disease Spirochetes Trends Microbiol. 28 (11): 889-899
Medina-Perez, D.N., Wager, B., Troy, E., Gao, L., Norris, S.J., Lin, T., Hu, L. T., Hyde, J.A., Lybecker, M., and. J.T. Skare. 2020. The intergenic small, non-coding RNA ittA is required for optimal infectivity and tissue tropism in Borrelia burgdorferi. PLoS Pathogens 16(5): e1008423.
Phelan, J.*, Ramsey, M.E.*, Kern, A.*, Lundt, M.E., Sharma, B., Lin, T., Gao, L., Norris, S.J., Hyde, J.A., Skare, J.T., and L. T. Hu. 2019. Genome-wide screen identifies novel genes required for Borrelia burgdorferi survival in its Ixodes tick vector. PLoS Pathogens 15(5): e1007644. PMCID: PMC6516651 *these co-authors contributed equivalently to this manuscript
Xie, J., Zhi, H., Garrigues, R.J., Keightly, A., Garcia, B.L., and T. Skare. 2019. Structural Determination of the Complement Inhibitory Domain of Borrelia burgdorferi BBK32 Provides Insight into Classical Pathway Complement Evasion by Lyme Disease Spirochetes. PLoS Pathogens 15(3): e1007659. PMCID: PMC6445466 Cited by the Faculty of 1000.
Zhi, H., Xie, J., and J.T. Skare. 2018. The Classical Complement Pathway is Required to Control Borrelia burgdorferi Levels During Experimental Infection. Front Immunol. 9:959. PMCID: PMC5949333
Hyde, J.A. and J.T. Skare. 2018. Detection of bioluminescent Borrelia burgdorferi from in vitro cultivation and during murine infection. Methods Mol Biol. 1690: 241-257. PMID: 29032549
Ramsey, M.E., Hyde, J.A., Medina-Perez, D.N., Lin, T., Gao, L., Lundt, M.E., Li, X., Norris, S.J., Skare, J. T., and L. Hu. 2017. A high-throughput genetic screen identifies previously uncharacterized Borrelia burgdorferi genes important for resistance against reactive oxygen and nitrogen species. PLoS Pathog. 13(2):e1006225
Skare, J.T., Shaw, D.K., Trzeciakowski, J.P., and J. A. Hyde. 2016. In vivo imaging demonstrates that Borrelia burgdorferi ospC is uniquely expressed temporally and spatially throughout experimental infection. PLoS One, 11(9): e0162501 .
Ebady, R., Katz, A., Boczula, A.E., Kim, Y.-R., Gupta, N., Tang, T., Odisho, T., Zhi, H., Simmons, C.A., Skare, J.T., and T. J. Moriarty. 2016. Biomechanics of Borrelia burgdorferi vascular interactions. Cell Reports, 16(10): 2593-2604.
Links to media coverage:
- Scientific American: "Something to Grapple with: How Wily Lyme Disease Prowls the Body"
- Science News: " Lyme bacteria swap "catch bonds" to navigate blood vessels"
- ScienMag: " How Lyme disease bacteria spread through the body"
- phys.org News: " How Lyme disease bacteria spread through the body"

Garcia B.L.*, Zhi, H.*, Wager, B, M. Höök, and J.T. Skare. 2016. Borrelia burgdorferi BBK32 Inhibits the Classical Complement Pathway by Blocking Activation of the C1 Complement Complex. PLoS Pathog 12(1): e1005404 .
*these co-authors contributed equivalently to this manuscript
Wager, B., Shaw, D.K., Groshong, A.M., Blevins, J.S., and J.T. Skare. 2015. BB0744 affects tissue tropism and spatial distribution of Borrelia burgdorferi. Infect Immun. 83(9): 3693-3703.
Zhi, H., Barbu, E.M., Weening, E.H., Hyde, J.A., Höök, M., and J.T. Skare. 2015. The BBA33 lipoprotein binds collagen and impacts Borrelia burgdorferi pathogenesis. Mol. Microbiol. 96(1): 68-83.
Moriarty, T. J., Shi, M., Lin, Y.-P., Ebady, R., Zhou, H., Odisho, T., Hardy, P.-O., Salman-Diligimen, A., Wu, J., Weening, E.H., Skare, J. T., Kubes, P., Leong, J., and G. Chaconas. 2012. Vascular binding of a pathogen under shear force through mechanistically distinct sequential interactions with host macromolecules. Mol Microbiol. 86(5): 1116-1131.
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.

Featured as a "Spotlight" Article in the March 2011 issue

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.
Featured as a "Spotlight" Article
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.
A MicroCommentary accompanied this article
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 burgdorferiLacking 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.
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.
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.
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

Lab Members

Research Scientists

Shannon Allen, Ph.D.
Lisa Funkhouser-Jones, Ph.D.

Graduate Students

Alexandra Powell
Brittany Shapiro

Undergraduates

Ayesha Nagaria
Haley Przespolewski
Payton Smith
Blez Arbolado
Natalie Brown