Elizabeth Rego
Yale University, CT·Microbiology & Immunology
Tuberculosis infects about 10 million people and kills nearly 1.5 million each year. It is hard to treat for two reasons.
- Fields
Microbiology & Immunology
Biochemistry
Biophysics
- Topics
tuberculosis
Mtb
cell envelope
- Grants
- 2 known grants, through Jul 2029
What they work on
- Track where and when Pks13, an enzyme that builds mycolic acids for the tuberculosis outer membrane, works inside cells and how it interacts with fatty acid synthases, using light and electron microscopy.
- Test whether the essential efflux pump EfpA acts as a lipid transporter in Mycobacterium tuberculosis, and explore whether blocking it could help existing antibiotics work better.
- Characterize PgfA and related proteins that coordinate outer-membrane building with balanced growth, using structural biology, cell biology and cryo-electron tomography.
- Identify which compartment inside host cells is most associated with tuberculosis drug tolerance, and which carbon source tolerant bacteria use, using single-cell growth and metabolism reporters and live-cell microscopy.
- Design lab culture conditions that mimic the environment of drug-tolerant M. tuberculosis, to support future screens for small molecules that kill these bacteria.
More about the research
First, the bacterium Mycobacterium tuberculosis (Mtb) is wrapped in a thick, multi-layered envelope that blocks many antibiotics. Second, some bacteria survive drugs without being genetically resistant. This work attacks both problems. One project studies how the envelope is built, so that disrupting it could make existing drugs work better. The other finds where drug-tolerant bacteria live inside host cells and what they feed on.
Why it matters
Tuberculosis patients often need long drug courses because the bacterial envelope blocks antibiotics and some bacteria tolerate treatment. Envelope-assembly proteins such as Pks13 and EfpA could become targets for structure-based drugs that boost current TB therapies. Culture conditions that mimic drug-tolerant bacteria could let screens find compounds that kill these hard-to-treat cells and could shorten treatment.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
James Chen
University of California-San Francisco, CA·Biophysics·Early-career
Purify the cell-wall proteins PonA1 and CrgA and their partner complexes directly from Mycobacterium tuberculosis and M. smegmatis, and determine their 3D structures by single-particle cryo-EM.
Bree Aldridge
Weill Medical College of Cornell University, NY·Microbiology & Immunology
Generate single-cell profiles of Mycobacterium tuberculosis responding to drug treatment and to gene knockdown, working with the four program projects on the treatments and genes each one studies.
Sadiya Parveen-Nesson
Louisiana State University, LA·Microbiology & Immunology
Test whether blocking glutaminase (GLS1), the enzyme that breaks down glutamine, restores the TB-killing ability of Mtb-infected macrophages, using siRNA knockdown, chemical inhibition and macrophages from macrophage-specific GLS1 knockout mice.
The school
Yale University: 73 labs on PI Pages, $1.5B a year on research, 438 research doctorates a year.
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