Regulation of DNA torsional stress at nuclear lamina
DNA transcription or replication creates torsional stress in the double helix. The enzyme that removes this stress is DNA topoisomerase I (Top1), a target of cancer chemotherapy. Loss of Top1 activity causes torsional stress accumulation in transcriptionally active genes and can lead to the formation of non-canonical DNA/RNA hybrid structures, called R loops. Recently, the project's team showed that depletion of Top1 leads to R loop stabilisation, specifically in genes anchored to the nuclear lamina. This observation strongly suggests that attachment of DNA to the nuclear lamina may prevent the dissipation of torsional stress. The EU-funded TorsionAtLamina project investigates the relationship between torsional stress, Top1, R loops and nuclear lamina attachment, employing genomics techniques developed in the host lab.
Fields of science
Call for proposalSee other projects for this call
Funding SchemeMSCA-IF - Marie Skłodowska-Curie Individual Fellowships (IF)
1066 CX Amsterdam
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