Microbiology, Molecular Genetics & Immunology
B.S. in Bacteriology, University of Wisconsin-Madison
M.S. in Food Science, University of Wisconsin-Madison
Ph.D. in Microbiology, University of Georgia
Postdoctoral Fellow, University of Nebraska Medical Center
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Office: 3009 Hixon | Lab: 4003 Wahl Hall West
913-588-7136 | email
Staphylococcus aureus is a gram-positive bacteria found commonly in the nares of humans. However, it is also a prolific pathogen that can cause an array of infections, ranging from mild skin and soft tissue infections to severe diseases such as toxic shock syndrome, scalded skin syndrome, necrotizing pneumonia, necrotizing fasciitis, abscesses, and endocarditis. While once considered an opportunistic pathogen, the recent emergence of particular CA-MRSA strains that can infect otherwise healthy individuals has challenged this notion. In a very simplistic view, S. aureus infections can be grouped in two categories: 1) acute invasive disease dependent on the production of secreted factors such as toxins, and 2) chronic infections associated with biofilm formation which may or may not form on implanted medical devices. The research of my lab focuses on dissecting the molecular mechanisms behind the ability of this bacterium to cause disease. Specifically, we have two projects summarized below.
AtlA murein hydrolase
This project continues studies of the Atl murein hydrolase (enzyme which cleaves peptidoglycan). Atl is the major murein hydrolase of Staphylococci and is an important enzyme in maintaining proper peptidoglycan structure and daughter cell separation. In addition, we and others have shown that this bifunctional enzyme is required for biofilm formation. Our current studies are focused on how this enzyme is regulated, how mutations in AtlA alter cell physiology, and how AtlA contributes to biofilm formation.
VfrAB in virulence factor regulation
We identified the vfrAB operon during a transposon screen for mutants defective in production of the major virulence factor α-hemolysin. Previously a hypothetical protein of unknown function found in all gram-positive bacteria, we determined that VfrB controls the production of numerous virulence factors including α-hemolysin and proteases. Interestingly, the ΔvfrB mutant shows increased pathogenesis in a dermonecrosis model of infection. We are currently dissecting the role of VfrB in virulence factor regulation, cellular metabolism, and virulence. To accomplish our studies, we are also heavily invested in the development of new genetic tools for studying S. aureus and closely related bacteria.
Select related publications:
Bose, J.L., S.M. Daly, P.R. Hall, and K.W. Bayles. 2014. Identification of the vfrAB operon in Staphylococcus aureus: a novel virulence factor regulatory locus. Infect. Immun. in press
Bose, J.L. 2014. Genetic manipulation of Staphylococci. In P.D. Fey (ed.), Staphylococcus epidermidis: Methods and Protocols. Springer Science + Business Media, LLC, New York, NY
Gries, C.M., J.L. Bose, A.S. Nuxoll, P.D, Fey, and K.W. Bayles. 2013. The Ktr potassium transport system in Staphylococcus aureus and its role in cell physiology, antimicrobial resistance, and pathogenesis. Mol. Microbiol. 89:760-773.
Bose, J.L., P.D. Fey, and K.W. Bayles. 2013. Genetic tools to enhance the study of gene function and regulation in Staphylococcus aureus. Appl. Environ. Microbiol. 79:2218-2224.
Fey, P.D., J.L. Endres, V.K. Yajjala, T.J. Widhelm, R.J. Boissy, J.L. Bose, and K.W. Bayles. 2013. A Genetic Resource for rapid and comprehensive screening of nonessential Staphylococcus aureus genes. mBio. 4(1):doi:10.1128/mBio.00537-12.
Bose, J.L., M.K. Lehman, P.D Fey, and K.W. Bayles. 2012. Contribution of the Staphylococcus aureus AtlA AM and GL murein hydrolase activities in cell division, autolysis, and biofilm formation. PloS ONE 7:e42244.
Kaplan, J.B., E.A. Izano, P. Gopal, M.T. Karwacki, S. Kim, J.L. Bose, K.W. Bayles, and A.R. Horswill. 2012. Low-levels of β-lactam antibiotics induce extracellular DNA release and biofilm formation in Staphylococcus aureus. mBio 3:e00198-12.
Jeffrey L. Bose, Ph.D.