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Trial Lecture – time and place
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Adjudication committee
- First opponent: Director of Research Olivier Espéli, Collège de France, France
- Second opponent: Professor Hanne Ingmer, University of Copenhagen, Denmark
- Third member and chair of the evaluation committee: Associate Professor Kay Oliver Schink, University of Oslo
Chair of the Defence
Associate Professor Nikolina Sekulic, University of Oslo
Principal Supervisor
Professor Emeritus Kirsten Skarstad, University of Oslo
Summary
Bacteria respond to antibacterial drug exposure by activating stress responses. These responses can promote survival and drive resistance development, thereby compromising antibacterial drug effectiveness. Studying bacterial stress responses is therefore essential for guiding measures that help ensure treatments remain effective.
The aim of this thesis was to investigate how bacteria rearrange their chromosome when exposed to severe DNA damage caused by antibacterial drugs. Using Escherichia coli exposed to the antibacterial drug ciprofloxacin as a model system, live-cell microscopy revealed an ordered two-step nucleoid rearrangement that culminates in a dense and persistent midcell compaction. This response, termed DNA supercompaction, was also observed after exposure to other DNA-damaging agents and across bacterial species, including clinical isolates, underscoring its broader biological relevance.
The genetic landscape of DNA supercompaction was explored through a genome-wide screening combined with machine learning-assisted analysis of compaction phenotypes. Key DNA repair proteins, RecA, RecBCD, and RecN, emerged as essential orchestrators of the response. Additionally, single-cell fluorescence imaging revealed a dynamic interplay between RecA and RecN at nucleoid-associated positions during DNA supercompaction.
Overall, this work identifies DNA supercompaction as an important and conserved component of the bacterial DNA damage response and provides a framework for future studies of this newly recognized layer of bacterial stress adaptation, which may prove relevant for preserving antibacterial drug effectiveness.
Additional information
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