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Primary Supervisor: Professor Madalena Tarsounas

Project Overview

Aberrant replication causes cells lacking BRCA2 to enter mitosis with under-replicated DNA, which activates a repair mechanism known as mitotic DNA synthesis (MiDAS). We have recently mapped genome-wide the sites where mitotic DNA synthesis (MiDAS) occurs in BRCA1/2-deficient cells (Groelly et al, Molecular Cell 2022), using state-of-the-art technologies (e.g. MiDAS-seq, high-content microscopy) and found that they co-localise with sites of R-loop formation. We now aim to investigate the roles of ATR/ATM kinases, as well as of MUS81 (Lai et al. Nat. Communications 2017) and other nucleases in regulating this process. Overall, this project combines cell/molecular biology and microscopy approaches with high-throughput technologies and bioinformatics to understand how BRCA1 and BRCA2 facilitate DNA replication and how this, in turn, impacts chromosome segregation during mitosis

Training Opportunities

  • cell/molecular biology;
  • high-content microscopy;
  • high-throughput sequencing technologies;
  • bioinformatics


  1. Groelly FJ, Fawkes M, Dagg RA, Blackford AN and Tarsounas M. 2022. Targeting DNA damage response pathways in cancer. Nature Reviews Cancer in press.
  2. Groelly FJ, Dagg RA, Petropoulos M, Rosetti G, Panagopoulos A, Paulsen T, Karamichali A, Jones SE, Ochs F, Dionellis VS, Puig-Lombardi E, Miossec MJ, Lockstone H, Legube G, Blackford AN, Altmeyer M, Halazonetis TD and Tarsounas M. 2022. Mitotic DNA synthesis is caused by transcription-replication conflicts in BRCA2-deficient cells. Molecular Cell 82: 3382-3397.