Food will be served from 12:00; the presentation starts at 12:15
Fluoroquinolone antibiotics like ciprofloxacin work by causing breaks in bacterial DNA, triggering repair mechanisms that can unfortunately promote antibiotic resistance. This resistance, especially in the common bacterium Escherichia coli (E. coli), poses a significant global health challenge.
Our research explores how E. coli's DNA physically responds to ciprofloxacin exposure. We've discovered a fascinating process we call "DNA supercompaction," where damaged DNA reorganizes into a dense structure at the center of the bacterial cell. This response occurs not only with fluoroquinolone antibiotics but also with other genotoxic agents.
Through live cell imaging, we found that two proteins are crucial for this process:
- RecN, a structural protein that helps maintain chromosome organization
- RecA, a key DNA repair protein
Our findings suggest these proteins work together as part of a universal survival strategy that bacteria employ when facing severe DNA damage. The intensity of this DNA compaction response correlates with the severity of DNA damage.
To identify additional genes involved in this process, we developed a machine learning algorithm trained to recognize DNA supercompaction in microscopy images. By screening over 3,000 bacterial mutants (each missing a single gene), we identified previously unknown genes that may play roles in this defense mechanism.