# overview
Jon Skare is Regents Professor and Associate Head of the Department of Microbial Pathogenesis and Immunology in the College of Medicine at Texas A&M University. He has been a faculty member at Texas A&M since 1996 and has led a research laboratory centered around the pathogenic mechanisms operative in Borrelia burgdorferi, the spirochetal bacterium that causes Lyme disease. He has published over 50 peer reviewed manuscript, reviews, and book chapters and been funded continuously by the NIH since 1999 with over $20 million dollars in total costs. Dr. Skare has trained ten graduate students, sixteen postdoctoral fellows, and numerous undergraduate students in his research group during his time at Texas A&M. The majority of his postdoctoral trainees and students have gone on to hold academic or industry positions in the medical sciences.

Research interests are focused on microbial pathogenesis with an emphasis in spirochetal infections, particularly Borrelia burgdorferi, the etiologic agent of Lyme disease. Broad training in the molecular biology, genetics, and biochemistry of prokaryotic systems is employed to answer research-related questions. Long-term interests in the lab are centered on understanding how B. burgdorferi promotes its pathogenic potential and persists in the disparate hosts it occupies in nature (e.g., both ticks and mammals). In this regard, the research program is aligned with: (i) regulatory pathways that contribute to the establishment of infection during the arthropod to mammalian transition; (ii) identifying and characterizing surface structures that contribute to the colonization and maintenance of infection via adherence mechanisms; and (iii) the ability of B. burgdorferi and relapsing fever Borrelia to persistently infect hosts in the face of a potent innate and adaptive immune response.

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Reverse Transcriptase Polymerase Chain Reaction

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5 Development Of Treatments And Therapeutic Interventions

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Reverse Transcriptase Polymerase Chain Reaction

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Reverse Transcriptase Polymerase Chain Reaction

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1.1 Normal Biological Development And Functioning

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Washington State University - (Pullman, Washington, United States)

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University of California Los Angeles - (Los Angeles, California, United States)

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University of California, Irvine - (Irvine, California, United States)

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College of Medicine, Research Excellence Award, Senior Division

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Borrelia burgdorferi lacking DbpBA exhibits an early survival defect during experimental infection.

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Analysis of mechanisms associated with loss of infectivity of clonal populations of Borrelia burgdorferi B31MI.

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A high-throughput genetic screen identifies previously uncharacterized Borrelia burgdorferi genes important for resistance against reactive oxygen and nitrogen species.

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Isolation of the outer membranes from Treponema pallidum and Treponema vincentii.

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Cloning and molecular characterization of plasmid-encoded antigens of Borrelia burgdorferi.

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Invasion of eukaryotic cells by Borrelia burgdorferi requires (1) integrins and Src kinase activity.

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Conformational dynamics of complement protease C1r inhibitor proteins from Lyme disease- and relapsing fever-causing spirochetes.

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Recombinant Treponema pallidum rare outer membrane protein 1 (Tromp1) expressed in Escherichia coli has porin activity and surface antigenic exposure.

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Virulent strain associated outer membrane proteins of Borrelia burgdorferi.

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American Society for Clinical Investigation

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The BBA33 lipoprotein binds collagen and impacts Borrelia burgdorferi pathogenesis.

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A Structural Basis for Inhibition of the Complement Initiator Protease C1r by Lyme Disease Spirochetes.

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The American Association of Immunologists

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Role of the TonB amino terminus in energy transduction between membranes.

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Characterization of a conditional bosR mutant in Borrelia burgdorferi.

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Escherichia coli TonB protein is exported from the cytoplasm without proteolytic cleavage of its amino terminus.

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Inactivation of the fibronectin-binding adhesin gene bbk32 significantly attenuates the infectivity potential of Borrelia burgdorferi.

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Transcriptional profiling of Borrelia burgdorferi containing a unique bosR allele identifies a putative oxidative stress regulon.

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Biomechanics of Borrelia burgdorferi Vascular Interactions.

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The intergenic small non-coding RNA ittA is required for optimal infectivity and tissue tropism in Borrelia burgdorferi.

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Borrelia burgdorferi gene expression profiling with membrane-based arrays.

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Decreased infectivity in Borrelia burgdorferi strain B31 is associated with loss of linear plasmid 25 or 28-1.

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The BB0646 protein demonstrates lipase and haemolytic activity associated with Borrelia burgdorferi, the aetiological agent of Lyme disease.

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Isolation and characterization of the outer membrane of Borrelia hermsii.

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Genome-wide screen identifies novel genes required for Borrelia burgdorferi survival in its Ixodes tick vector.

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Structure-function analysis of immunomodulatory lipoproteins from Borrelia miyamotoi

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Borrelia burgdorferi BBK32 Inhibits the Classical Pathway by Blocking Activation of the C1 Complement Complex.

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The Intergenic Small Non-Coding RNA ittA is Required for Optimal Infectivity and Tissue Tropism in Borrelia burgdorferi

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Identification of TonB homologs in the family Enterobacteriaceae and evidence for conservation of TonB-dependent energy transduction complexes.

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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.

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Minimal Role for the Alternative Pathway in Complement Activation By HIT Immune Complexes

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Evidence for a TonB-dependent energy transduction complex in Escherichia coli.

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The absence of linear plasmid 25 or 28-1 of Borrelia burgdorferi dramatically alters the kinetics of experimental infection via distinct mechanisms.

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Structural determination of the complement inhibitory domain of Borrelia burgdorferi BBK32 provides insight into classical pathway complement evasion by Lyme disease spirochetes.

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A conservative amino acid change alters the function of BosR, the redox regulator of Borrelia burgdorferi.

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In Vivo Imaging Demonstrates That Borrelia burgdorferi ospC Is Uniquely Expressed Temporally and Spatially throughout Experimental Infection.

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A novel fibronectin binding motif in MSCRAMMs targets F3 modules.

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Porin activity of the native and recombinant outer membrane protein Oms28 of Borrelia burgdorferi.

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Complement Evasion by Lyme Disease Spirochetes.

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BB0744 Affects Tissue Tropism and Spatial Distribution of Borrelia burgdorferi.

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The Oms66 (p66) protein is a Borrelia burgdorferi porin.

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A structural basis for inhibition of the complement initiator protease C1r by Lyme disease spirochetes

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Minimal role for the alternative pathway in complement activation by HIT immune complexes.

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Rabbit model of Lyme borreliosis: erythema migrans, infection-derived immunity, and identification of Borrelia burgdorferi proteins associated with virulence and protective immunity.

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American Society for Clinical Investigation

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Energy transduction between membranes. TonB, a cytoplasmic membrane protein, can be chemically cross-linked in vivo to the outer membrane receptor FepA.

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VraA (BBI16) protein of Borrelia burgdorferi is a surface-exposed antigen with a repetitive motif that confers partial protection against experimental Lyme borreliosis.

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Detection of Bioluminescent Borrelia burgdorferi from In Vitro Cultivation and During Murine Infection.

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Dissolved oxygen levels alter gene expression and antigen profiles in Borrelia burgdorferi.

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Borrelia burgdorferi alters its gene expression and antigenic profile in response to CO2 levels.

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Profiling of temperature-induced changes in Borrelia burgdorferi gene expression by using whole genome arrays.

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"Conformational dynamics of C1r inhibitor proteins from Lyme disease and relapsing fever spirochetes".

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The Classical Complement Pathway Is Required to Control Borrelia burgdorferi Levels During Experimental Infection.

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Genetic transformation of Borrelia burgdorferi.

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Comparison of protection in rabbits against host-adapted and cultivated Borrelia burgdorferi following infection-derived immunity or immunization with outer membrane vesicles or outer surface protein A.

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Sequence analysis and characterization of a 40-kilodalton Borrelia hermsii glycerophosphodiester phosphodiesterase homolog.

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Vascular binding of a pathogen under shear force through mechanistically distinct sequential interactions with host macromolecules.

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Borrelia miyamotoi FbpA and FbpB Are Immunomodulatory Outer Surface Lipoproteins With Distinct Structures and Functions.

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Bioluminescent imaging of Borrelia burgdorferi in vivo demonstrates that the fibronectin-binding protein BBK32 is required for optimal infectivity.

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A 9.0-kilobase-pair circular plasmid of Borrelia burgdorferi encodes an exported protein: evidence for expression only during infection.

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A mutation in the amino terminus of a hybrid TrpC-TonB protein relieves overproduction lethality and results in cytoplasmic accumulation.

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Regulatory Pathways in Borrelial Pathogenesis

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National Institute of Allergy and Infectious Diseases - (Bethesda, Maryland, United States)

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Virulence Mechanisms of Multifunctional Borrelial Proteins

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National Institute of Allergy and Infectious Diseases - (Bethesda, Maryland, United States)

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Virulence Mechanisms of Multifunctional Borrelial Proteins (Skare, Jon)

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National Institute of Allergy and Infectious Diseases - (Bethesda, Maryland, United States)

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A novel antimicrobial resistance mechanism for Borrelia burgdorferi

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National Institute of Allergy and Infectious Diseases - (Bethesda, Maryland, United States)

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Geneitc Mechanisms in Borrelia burgdorferi Pathogenesis

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National Institute of Allergy and Infectious Diseases - (Bethesda, Maryland, United States)

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Characterization of Virulent Strain Associated and in vivo Expressed Antigens of Borrelia burgdorferi

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American Heart Association - (New York, New York, United States)

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An Intracelluar Niche for Borrelia burgdorferi

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National Institute of Allergy and Infectious Diseases - (Bethesda, Maryland, United States)

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Collagen Binding as a Virulence Mechanism in Lyme Borreliosis

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National Institute of Allergy and Infectious Diseases - (Bethesda, Maryland, United States)

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A New Mammalian-Specific Function for OspC in Lyme Borreliosis

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National Institute of Allergy and Infectious Diseases - (Bethesda, Maryland, United States)

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The Role of Small Non-coding RNA in Borrelial Pathogenesis

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National Institute of Allergy and Infectious Diseases - (Bethesda, Maryland, United States)

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Host Spirochete Interactions in Lyme Disease

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National Institute of Allergy and Infectious Diseases - (Bethesda, Maryland, United States)

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Coping with Stress: Next Generation Approaches to Borrelia burgdorferi Host Adaptation

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National Institute of Allergy and Infectious Diseases - (Bethesda, Maryland, United States)

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Surface Proteins and Spirochetal Infections

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National Institute of Allergy and Infectious Diseases - (Bethesda, Maryland, United States)

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Classical Complement Pathway Evasion Mechanisms of Lyme Disease Spirochetes

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National Institute of Allergy and Infectious Diseases - (Bethesda, Maryland, United States)

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Texas A&M Health Science Center; Microbial Pathogenesis and Immunology; 1359 TAMUS

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Medina, Diana Natalie (2019-10). Characterization of Novel Small Regulatory RNAs In Borrelia burgdorferi and Their Role in Lyme Disease Pathogenesis. Doctoral Dissertation.

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Powell, Alexandra Daniela (2023-05). Inhibition of the Complement Classical Pathway as an Immune Evasion and Survival Technique Across Borrelia Species. Doctoral Dissertation.

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Zhi, Hui (2016-08). Deciphering Novel Functions of Borrelia Burgdorferi Surface Proteins and Their Potential Roles in Borrelial Pathogenesis. Doctoral Dissertation.