Stephanie Seveau
Ohio State University, OH·Microbiology & Immunology
A cell's outer membrane is easily torn by physical force or punctured by chemicals and bacterial toxins. Cells survive by quickly resealing these holes.
- Fields
Microbiology & Immunology
Biology
Biochemistry
- Topics
plasma membrane repair
pore-forming toxins
cholesterol-dependent cytolysins
- Grants
- 2 known grants, through May 2031
What they work on
- Map the spatiotemporal dynamics and molecular architecture of septin repair domains, from injury to resealing, in cells damaged by toxins or mechanical wounding, using super-resolution and FRET microscopy.
- Test how septins mediate plasma membrane repair, including whether they act as scaffolds for repair proteins, and identify septin partner proteins during repair using unbiased proteomics.
- Define how septin-dependent repair pathways affect host cell invasion by Listeria monocytogenes and disease severity, using a mouse infection model.
- Determine how plasma membrane depolarization organizes calcium-dependent lysosome exocytosis, which releases protective cathepsin enzymes onto the cell surface, after listeriolysin O perforation.
- Identify the targets of conventional PKC enzymes activated by LLO pores using SILAC quantitative proteomics, and test how they help Listeria escape its vacuole into the cytosol.
- Test whether low-grade membrane perforation, through potassium efflux and NLRP3 inflammasome activation, drives antigen-presenting cell maturation and stronger T cell immunity, in vitro and in mice.
More about the research
Calcium rushing in through a wound is known to trigger repair, but the steps that follow are poorly understood. The lab studies this repair process using bacterial toxins that punch holes in membranes. It also asks how these holes affect infection by Listeria monocytogenes, a foodborne bacterium that causes the life-threatening disease listeriosis.
Why it matters
Many bacteria, including those that cause listeriosis and pneumonia, damage host cells with pore-forming toxins. Understanding how cells repair membranes and how the immune system responds could guide new vaccines and therapies for these infections. It could also inform treatments for other diseases involving excessive membrane damage or faulty repair.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Sarah E. F. D'Orazio
University of Kentucky, KY·Microbiology & Immunology
Determine whether the route neurotropic Listeria monocytogenes use to cross the gut lining, or the inflammation they provoke, concentrates them in nerve bundles of the intestinal submucosa or in vagal nerve endings near gut lymphoid cryptopatches.
Patricia A Champion
University of Notre Dame, IN·Microbiology & Immunology
Identify how Mycobacterium marinum senses the detergent tyloxapol, combining unbiased genetic screens with hemolysis assays, and test whether tyloxapol suppresses ESX-1 membrane-breaking activity during macrophage infection.
Egil Lien
University of Massachusetts Chan Medical School, MA·Microbiology & Immunology
Determine how loss of the splicing factors Raver1 or Ptbp1 changes RIPK1/caspase-8-driven cell death and inflammation, using knockout macrophages and other cell lines infected with Yersinia.
The school
Ohio State University: 71 labs on PI Pages, $1.6B a year on research, 882 research doctorates a year.
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