Jeonghoon Lee
University of Nebraska Medical Center, NE·Microbiology & Immunology
Chlamydia trachomatis causes one of the most common sexually transmitted bacterial infections in the world. Infections frequently produce no symptoms, which helps them spread unnoticed, and untreated infection in women can lead to pelvic inflammatory disease, ectopic pregnancy and infertility.
- Fields
Microbiology & Immunology
Biochemistry
- Topics
Chlamydia trachomatis
sexually transmitted infection
bacterial cell division
- Grants
- 1 known grant, through Jul 2028
What they work on
- Test whether Pkn1, a serine/threonine kinase of Chlamydia trachomatis, controls recruitment of cell-division components to the septum, using an anhydrotetracycline-inducible, histidine-tagged Pkn1 and CRISPR interference knockdown of pkn1.
- Determine whether Pkn1's own phosphorylation state dictates whether it sits in the cytosol or at the division septum, by comparing catalytically inactive Pkn1 constructs with the active, tagged protein in infected cells.
- Identify proteins that bind Pkn1 using bacterial adenylate cyclase two-hybrid (BACTH) screening, then confirm the interactions with pull-down and co-immunoprecipitation assays.
- Confirm which interacting proteins are genuine Pkn1 substrates through in vitro kinase assays and phosphoprotein staining of SDS-PAGE gels, building a map of Pkn1 phosphorylation signaling.
More about the research
The bacterium lives only inside host cells and has a reduced genome with just eight transcription factors, the proteins that normally switch genes on and off. Yet its two-stage life cycle inside the cell is tightly timed. That mismatch suggests the bacterium controls its cycle largely after genes are read, by chemically modifying proteins. This project focuses on one such modification, phosphorylation, the attachment of phosphate groups that acts as an on-off switch for protein activity.
Why it matters
Chlamydia trachomatis infections are widespread and often silent, and in women can progress to pelvic inflammatory disease, ectopic pregnancy and infertility. Because the bacterium must divide to complete its infectious cycle, the proteins that control division are candidate drug targets. Identifying what Pkn1 does and which proteins it modifies could point toward new therapeutic strategies against chlamydial disease.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Kathryn Frietze
University of New Mexico, NM·Microbiology & Immunology
Engineer bacteriophage virus-like particle vaccines, virus shells that display a chosen protein fragment in a repeating array, to raise high levels of antibodies against Chlamydia trachomatis adhesion factors, and measure their immunogenicity in mouse immunization studies.
Mary Weber
University of Iowa, IA·Microbiology & Immunology
Determine mechanistically how the Chlamydia trachomatis effector TmeA regulates N-WASP, a host trigger of actin assembly, and whether this interaction drives membrane ruffling, pedestal formation and filopodial dynamics during invasion.
William Geisler
University of Alabama at Birmingham, AL·Medicine & Clinical Research·Early-career
Determine whether the HLA-DQB1*06 gene variant and chlamydia-specific CD4+ IFN-gamma responses from helper T cells can predict new Chlamydia trachomatis infections in women, to guide testing frequency.
The school
University of Nebraska Medical Center: 20 labs on PI Pages, $657M a year on research, 82 research doctorates a year.
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