Shelley Payne
University of Texas at Austin, TX·Microbiology & Immunology
A bacterium that causes dysentery has to survive a gauntlet: the acid and nutrients of the gut, a thick mucus layer, and then the inside of the cells lining the intestine. How does it know where it is, and how does it switch on the right genes at the right moment?
- Fields
Microbiology & Immunology
Biology
Genetics
- Topics
Shigella flexneri
shigellosis
dysentery
- Grants
- 1 known grant, through Jun 2030
What they work on
- Determine how carbon-source availability tells Shigella flexneri where it is in the host, by testing mutants defective in specific carbon metabolism pathways for invasion, intracellular replication, and cell-to-cell spread in human cells.
- Test the role of carbon-status signaling relays, including the starvation alarm molecule ppGpp and the mRNA-binding regulator CsrA, in switching on virulence genes during infection of cultured human cells and intestinal organoids.
- Map which bacterial and human genes change during infection using dual RNA-Seq on infected human intestinal organoids, and use the results to build additional mutants for functional testing.
- Determine how S. flexneri evades the protective effects of type I interferon (IFN-β) on host cells, and why bacteria that do invade spread faster and form larger lesions when interferon is present.
More about the research
Work here centers on Shigella flexneri, an intestinal pathogen responsible for millions of dysentery cases a year, and on the idea that the bacterium reads its surroundings by sensing which sugars and other carbon sources are available.
Why it matters
Bacterial intestinal infections are a leading cause of illness and death worldwide, and Shigella alone causes millions of dysentery cases each year. Identifying the signals this pathogen uses to maximize growth in the gut and to dodge innate immune clearance could reveal targets for drugs or preventive strategies that work differently from antibiotics — an important option as antibiotic-resistant strains spread.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Leigh Knodler
University of Vermont, VT·Microbiology & Immunology
Determine whether nine genes in the 40-kilobase type III secretion gene cluster on the Providencia alcalifaciens plasmid drive invasion of host cells, combining computational prediction, in vitro biochemistry and infection of cultured non-phagocytic cells.
Madison Collins
Montana State University, MT·Microbiology & Immunology
Test the hypothesis that molecules controlled by the S. aureus SaeR/S gene regulatory system disrupt autophagy, a self-digestion process that kills trapped microbes, in human neutrophils after they swallow the bacteria.
Gustavo Caballero Flores
University of Wisconsin-Madison, WI·Microbiology & Immunology·Early-career
Identify bacterial factors that Citrobacter rodentium needs to establish bacteremia, bloodstream infection, in newborn mice, using genome-wide mutant screens followed by functional testing of candidates in live animals.
The school
University of Texas at Austin: 49 labs on PI Pages, $1.1B a year on research, 871 research doctorates a year.
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