Mechanisms of double-strand break repair pathway choice

DNA double-strand breaks (DSBs) are a major threat to genome stability, as failure to repair them correctly can give rise to chromosome translocations and genome amplification events and is the underlying cause of a number of hereditary cancer predisposition syndromes, such as Fanconi anaemia. The two main pathways for the repair of DSBs are non-homologous end joining and homologous recombination. Dr Boulton will be investigating the role of the protein 53BP1 in the regulation of DSB repair, with the goal of gaining a molecular understanding of how 53BP1 and its cofactors bind and protect DNA ends.