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Matthew Mulvey


Graduate Program Membership:

Office/Building: CSC 224A
Phone: 801-581-5967
Mulvey Lab: Coming Soon

Research Statement

The Mulvey lab aims to define mechanisms by which pathogenic strains of Escherichia coli colonize diverse host niches, persist, and spread in the face of numerous environmental stresses, innate and adaptive host defenses, aggressive competition with other microbes, and exposure to antibiotics. We are especially interested in understanding how intraspecies genetic diversity and bacterial adaptive responses impact host-microbe interactions and the manifestation of variable disease phenotypes. Much of our work is focused on Extraintestinal Pathogenic Escherichia coli (ExPEC), which are leading causes of urinary tract and bloodstream infections. We have also recently initiated studies to define the pathogenic and survival mechanisms of diarrheagenic strains of E. coli, which are especially problematic and often lethal for children in developing countries. Our ongoing research indicates that even closely related bacterial strains can vary markedly in their ability to cause disease, dependent in part on host and environmental cues, input from neighboring microbes (the microbiota), and the specific gene sets carried by individual pathogens. To understand how environmental and evolutionary forces shape host-pathogen interactions, my lab employs a variety of experimental approaches and disciplines, including microbiology, microscopy, cell and molecular biology, biochemistry, bioinformatics, genetics, and genomics, as well as cell culture, mouse, and zebrafish models of localized and systemic infections. We also work closely with clinicians and bioinformaticists to identify and functionally define specific bacterial factors that impact the onset, progression, severity, and outcomes of diseases, including intestinal, urinary tract, and bloodstream infections.

Research Interests

General Interests

Selected Publications

  • Complete list of published work in MyBibliography:
  • 1. Fleming BA*, Blango MG*, Rousek AA*, Kincannon WM, Tran A, Lewis AJ, Russell CW, Zhou Q, Baird LM, Barber AE, Brannon JR, Beebout CJ, Bandarian V, Hadjifrangiskou M, Howard MT, Mulvey MA (2022). A tRNA modifying enzyme as a regulatory nexus for control of bacterial stress responses and virulence. Nucleic Acids Res. gkac116. doi: 10.1093/nar/gkac116. PMCID: PMC9303304. *equal contributors. **Press related to this paper includes:
  • 2. Forde BM, Roberts LW, Phan M-D, Peters KM, Fleming BA, Russell CW, Lenherr SM, Myers JB, Barker AP, Fisher MA, Chong T-M, Yin WF, Chang KG, Schembri MA*, Mulvey MA*, Beatson SA (2019). Population Dynamics of an Escherichia coli ST131 Lineage during Recurrent Urinary Tract Infection. Nature Comm., 10(1):3643. doi: 10.1038/s41467-019-11571-5. PMCID: PMC6692316. *Co-corresponding authors. **Press related to this paper includes an article by S. Zhang in The Atlantic, Sept 3, 2019,
  • 3. Russell CW, Fleming BA, Jost CA,Tran A, Stenquist AT, Wambaugh MA, Bronner MP, Mulvey MA (2018). Context-dependent Requirements for FimH and Other Canonical Virulence Factors in Gut Colonization by Extraintestinal Pathogenic Escherichia coli. Infect Immun. 86(3): pii: e00746-17. PMCID:PMC5820936.
  • 4. Dhakal BK and Mulvey MA (2012). The UPEC pore forming toxin a-hemolysin triggers proteolysis of host proteins to disrupt cell adhesion, inflammatory and survival pathways. Cell Host Microbe 11:58-69. PMC3266558. **Press related to this paper includes: - WBUR (Boston NPR station) CommonHealth: - Highlighted by Faculty of 1000 Biology. - Justice SS and Hunstad DA (2012). UPEC Hemolysin: More than Just for Making Holes. Cell Host Microbe. 11:4-5.
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Courses Taught

  • BIOL 5210, Cell Structure and Function
  • Dent 7135, Host and Defense, Bacterial Pathogenesis