Craig D Ellermeier
University of Iowa, IA·Microbiology & Immunology
Clostridioides difficile is a gut bacterium. It causes nearly 500,000 colon infections and about 30,000 deaths a year in the United States, and the CDC rates it an urgent public health threat.
- Fields
Microbiology & Immunology
Genetics
Biochemistry
- Topics
Clostridioides difficile
Clostridium difficile
C. difficile infection
- Grants
- 2 known grants, through Jul 2027
What they work on
- Identify which enzymes form the unusual 3-3 and the common 4-3 peptidoglycan crosslinks in the C. difficile cell wall, and how their ratio is regulated, using genetics, biochemistry and microscopy.
- Assign about 50 putatively essential cell envelope genes to functional pathways using CRISPR interference (CRISPRi), a gene-silencing tool, and characterize a new transcriptional regulatory system found in a pilot screen.
- Define how the DraRS two-component system, a bacterial sensor-and-response pair, controls resistance to daptomycin and other envelope stresses, by testing gain- and loss-of-function mutants and mapping the genes DraR regulates.
- Test whether DraRS is activated when antibiotics disrupt the lipid II cell-wall precursor cycle, by using CRISPRi to mimic antibiotic effects and isolating DraS mutants that cannot sense stress.
- Determine how DapRS and its target genes hexSDF make an unusual membrane glycolipid, and how they affect daptomycin resistance, cell surface charge and lipid content.
More about the research
The infections are hard to treat for two reasons. The bacterium forms dormant spores that survive antibiotics. And the antibiotics used against it also kill healthy gut bacteria, which clears the way for C. difficile to return. Many of the most useful antibiotics target the cell envelope, the wall and membrane layers that surround a bacterium. Both projects study how C. difficile builds this envelope and how it defends it when antibiotics attack. The goal is to find weak points that new, more selective drugs could target.
Why it matters
C. difficile infections kill tens of thousands of Americans each year, mainly in hospitals and nursing homes, and current antibiotics also wipe out protective gut bacteria. By identifying unusual cell-wall enzymes, essential envelope genes, and the stress-response systems behind resistance to daptomycin and vancomycin, this work could point to new drug targets that treat C. difficile more selectively.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Michael Stephen Trent
University of Georgia, GA·Microbiology & Immunology
Develop an analytical tool that measures LPS molecules in transit, and combine it with mass spectrometry of the enzyme LpxC and LPS precursors to determine how the YejM-YciM system controls LPS production in E. coli.
Jenessa Winston
Ohio State University, OH·Microbiology & Immunology·Early-career
Test whether daily supplementation with the secondary bile acid ursodeoxycholic acid (UDCA) changes susceptibility to and severity of Clostridioides difficile infection in IL10-knockout colitis mice.
Christopher Brown
Weill Medical College of Cornell University, NY·Microbiology & Immunology·Early-career
Expose laboratory and clinical strains of Mycobacterium tuberculosis to air-drying stress and document the resulting changes in metabolism and cell envelope integrity.
The school
University of Iowa: 32 labs on PI Pages, $703M a year on research, 418 research doctorates a year.
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