Click here to stream the public defence
Due to copyright issues, an electronic copy of the thesis must be ordered from the faculty. For the faculty to have time to process the order, the order must be received by the faculty at the latest 2 days before the public defence. Orders received later than 2 days before the defence will not be processed. After the public defence, please address any inquiries regarding the thesis to the candidate.
Trial Lecture – time and place
See Trial Lecture.
Adjudication committee
- First opponent: Professor Jeremy Carlton, King's College, The Francis Crick Institute, UK
- Second opponent: Group Leader Randi Gussgard Syljuåsen, Institute for Cancer Research, Oslo University Hospital, Norway
- Third member and chair of the evaluation committee: Associate professor Tor Erik Rusten, University of Oslo
Chair of the Defence
Professor Vessela Kristensen, University of Oslo
Principal Supervisor
Associate Professor Coen Campsteijn, University of Oslo
Summary
The genome of eukaryotic cells resides in the nucleus and is protected by the nuclear envelope, a double membrane that regulates exchange between nucleus and cytoplasm while safeguarding genetic material. Once considered a passive barrier, the nuclear envelope is now known to be highly dynamic: it disassembles and reassembles during cell division, adapts to growth, responds to mechanical stress, and repairs after damage. Disruption of these processes compromises genome stability, triggers inflammatory responses, and contributes to disease.
This thesis investigates mechanisms that maintain nuclear envelope integrity and explores how their failure affects cell fitness and fate. It shows that nuclear envelope repair relies on precisely coordinated molecular pathways that detect membrane breaches and confine repair to affected regions. Loss of control increases chromatin stress and DNA damage, undermining cell fitness.
This work also reveals that mutations in the nuclear lamina raise sensitivity to mechanical stress. In adipocytes, intracellular lipid accumulation exacerbates nuclear deformation and nuclear envelope damage, causing impaired function, DNA damage, and inflammatory responses. Finally, proteins classically linked to stress responses are shown to support accurate chromosome segregation during mitosis, and their dysfunction promotes chromosome missegregation and genomic instability.
Together, these findings position the nuclear envelope as an active regulator of genome protection and provide insight into cancer and inherited nuclear envelope disorders.
Additional information
Contact the research support staff.