How a bacterial enzyme helps germs quickly become resistant to antibiotics
An Analysis of ICE R391 Pathogen-encoded Rum DNA Polymerase in Generating Mutations Driving Rapid Acquisition of Antibiotic Drug Resistance in Diverse Recipient Bacterial Species
This project explains how a bacterial enzyme causes germs to mutate and become resistant to antibiotics, which could help people with infections that don't respond to medicines.
Quick facts
| Grant type | R01 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | University of Southern California NIH-funded |
| Lab location | 1 site (Los Angeles, UNITED STATES) |
| Project ID | NIH-11304577 on NIH RePORTER |
What this research studies
Researchers will grow different bacterial species in the lab and introduce the R391 mobile element that carries the Rum DNA polymerase to see how it changes bacterial DNA. They will change and test the bacterial RecA protein, focusing on a specific methionine (M197), to learn how it teams up with Rum pol to create mutations. The team will use DNA sequencing to map where mutations happen and will test whether those mutations make bacteria resistant to common antibiotics. Results will be compared across several recipient species to determine how broadly this mechanism speeds up antibiotic resistance.
Who could benefit from this research
Good fit: People with infections that don't respond to standard antibiotics are the group most likely to benefit from insights produced by this work.
Not a fit: Patients with non-bacterial illnesses or infections not driven by antibiotic resistance are unlikely to receive direct benefit from this laboratory-focused research.
Why it matters
Potential benefit: If successful, this work could reveal a common mechanism that drives rapid antibiotic resistance and point to ways to prevent or slow resistance, helping future patients get more effective treatments.
How similar studies have performed: Related research has shown that error-prone polymerases can drive mutations and resistance, but the specific role of Rum pol across diverse bacterial species and the RecA M197 interaction is less well tested.
Where this research is happening
Los Angeles, UNITED STATES
- University of Southern California — Los Angeles, United States (Active)
Researchers
- Principal investigator: Goodman, Myron — University of Southern California
- Study coordinator: Goodman, Myron
About this research
- This is an active NIH-funded research project — typically early-stage science, not a clinical trial accepting patient enrollment.
- Some NIH-funded labs run parallel clinical studies or seek volunteers for related work. To check, contact the principal investigator or institution listed above.
- For full project details, budget, and progress reports, visit the official NIH RePORTER page below.