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Postdoctoral Research Fellow
Address: 3-401 BSB
Phone: (319) 335-7817
Mentor: Wilmara Salgado-Pabón, PhD
Undergraduate Institution: University of Rochester
PhD Institution: University of Pittsburgh
Staphylococcus aureus is a common human pathogen capable of causing a variety of diseases ranging from minor skin infections to potentially fatal infections such as necrotizing pneumonia and endocarditis. The emergence of antibiotic resistant strains, such as methicillin-resistant Staphylococcus aureus (MRSA), has significantly complicated treatment of these conditions and led to growing concern regarding future infections. In order to combat the continued evolution of drug resistance in this organism, a detailed understanding of the physiology and mechanisms of pathogenesis is required. Additional studies on S. aureus will contribute to our knowledge of this deadly pathogen and may reveal novel virulence mechanisms and exploitable therapeutic targets.
Epigenetic modification of DNA through methylation is utilized by a variety of organisms to provide an additional layer of regulatory information to the standard four nucleotide sequence. This base pair modification can modulate the rate of transcription in methylated regions and additionally can facilitate or prevent DNA-protein interactions. The development of single-molecule real time (SMRT) sequencing, a next-generation sequencing platform, allows for generation of a genome-wide analysis of methylation (“the methylome”) in bacteria.
The nature and significance of epigenetic modification in Staphylococcus aureus remains occluded. Currently, I am working on expanding our knowledge of DNA methylation in this organism through the use of next-generation sequencing, bacterial genetics, and molecular biology. It is my hope that the study of S. aureus DNA methylation patterns will shed light on an important, yet unstudied, aspect of S. aureus physiology.
Brown MJ, Russo BC, O’Dee DM, Schmitt DM, Nau GJ. (2014) The contribution of the glycine cleavage system to the pathogenesis of Francisella tularensis. Microbes and Infection Apr;16(4):300-9
Russo BC, Brown MJ, Nau GJ. (2013) MyD88 prolongs survival and reduces bacterial burden during pulmonary infection with virulent Francisella tularensis. American Journal of Pathology Oct;183(4):1223-32
Schmitt DM, O’Dee DM, Brown MJ, Horzempa J, Russo BC, Nau GJ (2013) Role of NK cells in host defense against pulmonary type A Francisella tularensis infection. Microbes and Infection Mar;15(3):201-11
Schmitt DM, O’Dee DM, Horzempa J, Carlson PE, Russo BC, Bales J, Brown MJ, Nau GJ (2012) A Francisella tularensis live vaccine strain that improves stimulation of antigen presenting cells does not enhance vaccine efficacy. Plos One 7(2): e31172
Russo BC, Horzempa J, O’Dee DM, Schmitt DM, Brown MJ, Carlson PE, Xavier RJ, Nau GJ (2011) A Francisella tularensis locus required for spermine responsiveness is necessary for virulence. Infection and Immunity 79:3665-3676
Horzempa J, Shanks RM, Brown MJ, Russo BC, O’Dee DM, Nau GJ (2010) Utilization of an unstable plasmid and the I-Sce1 endonuclease to generate routine markerless deletion mutants in Francisella tularensis. Journal of Microbiological Methods 80:106-108
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