The role of proteins that are central to RAD51 loading in homologous recombination are also important in the protection of stalled replication forks from degradation by nucleases. Many of these act to promote RAD51 accumulation on single-stranded DNA that is exposed. Evidence that protection of replication forks is more than a form of RAD51-loading is emerging. Here Prof Morris will discuss recent work revealing the regulation of BRCA1 in replication fork protection and how it differs from that in promoting recombination in HR. The work also raises questions about the role of fork protection in cancer predisposition.
- Appreciation of the role of BRCA1 in homologous recombination DNA repair.
- The surprising different requirement of BRCA1 in replication fork protection
- Speculation about the role in cancer predisposition.
Professor Jo Morris set up her lab at the University of Birmingham in the United Kingdom in 2010. Jo has interests in post-translation systems and how they relate to the regulation of mammalian DNA repair and replication. Her recent work relates to how the removal of SUMO is critical for the correct timing of events in DNA repair and how the addition and removal of ubiquitin, by BRCA1 and USP48 respectively, control 53BP1 placement and resection. Recently her interest in post-translational recombination has extended to the role of proline isomerisation in replication.