Mary Weber
University of Iowa, IA·Microbiology & Immunology
Certain bacteria can only live inside human cells, and to get in and stay in they inject proteins, called effectors, that rewire the cell's machinery. Work in this group centers on how two such pathogens do this.
- Fields
Microbiology & Immunology
Biology
Medicine & Clinical Research
- Topics
Chlamydia trachomatis
Orientia tsutsugamushi
scrub typhus
- Grants
- 4 known grants, through Jul 2030
What they work on
- 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.
- Dissect the interplay among the secreted effectors TarP, TepP and TmeA and test whether additional effectors made only in the infectious elementary body are required for entry into non-phagocytic cells.
- Use cryo-electron microscopy to establish how Rab GTPase-CpoS-Inc interactions mediate fusion between chlamydial inclusions and with host vesicles, testing whether CpoS mimics SNARE membrane-fusion proteins.
- Define how the inclusion membrane protein IncC disrupts host vesicle trafficking to keep the Chlamydia-containing vacuole from being delivered to degradative compartments.
- Test with proteomics and advanced microscopy whether the effector CteG uses Sfi1-like motifs to bind the C-terminus of centrin-2, displacing its normal partners and causing cells to accumulate extra centrosomes.
- Use newly generated Chlamydia null strains to determine whether the bacterium blocks centrosome duplication and host cytokinesis to enhance its release by extrusion, and test in cellular and in vivo models whether these abnormalities promote cellular transformation.
- Create the first genetic transformation system for Orientia tsutsugamushi, including a shuttle vector and transformation method, and adapt TargeTron to insertionally inactivate selected tetratricopeptide repeat proteins.
- Use the new Orientia mutants to test whether specific tetratricopeptide repeat proteins are secreted and whether they promote host cell invasion or bacterial proliferation by perturbing the host cell cycle.
More about the research
Chlamydia trachomatis is the most common bacterial sexually transmitted infection worldwide and the leading cause of non-congenital blindness, with no vaccine and frequent reinfection. Orientia tsutsugamushi causes scrub typhus, a mite-borne disease that infects over a million people a year and can be fatal. Three projects dissect how Chlamydia forces entry into cells, builds and protects its intracellular compartment, and disturbs the machinery that divides cells. A fourth project builds the genetic tools needed to study Orientia at all.
Why it matters
Chlamydia trachomatis causes blindness and infertility and raises the risk of cervical and ovarian cancer, with no vaccine available. Mapping the bacterial proteins that drive entry, protect the replicative compartment and derange cell division could identify targets for blocking infection and clarify whether infection primes cells for cancer, which matters for women's health. For scrub typhus, which kills without treatment and is spreading beyond its traditional range, the first genetic tools would remove the main barrier to understanding how the pathogen causes disease.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Functional characterization of Chlamydia trachomatis inclusion membrane proteins and their role in subversion of the host vesicular trafficking
NIH · Apr 2020 – Jul 2030
Centrosome Subversion by Chlamydial Effectors: Implications for Cellular Transformation and Oncogenesis
NIH · Jun 2026 – May 2030
Development of genetic tools for overexpression and targeted mutagenesis of Orientia tsutsugamushi TPR proteins
NIH · Jan 2024 – Dec 2026
Closest labs
Jeonghoon Lee
University of Nebraska Medical Center, NE·Microbiology & Immunology
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.
Maria Lara-Tejero
Yale University, CT·Microbiology & Immunology
Determine the structure of the Salmonella type III secretion sorting platform, the part of the injectisome inside the bacterium, using cryo-EM and cryo-electron tomography.
Jorge E Galan
Yale University, CT·Microbiology & Immunology
Determine how short N-terminal secretion signals and dedicated chaperones direct client proteins to the type III secretion injectisome, the syringe-like machine Salmonella uses to inject proteins into host cells.
The school
University of Iowa: 32 labs on PI Pages, $703M a year on research, 418 research doctorates a year.
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