Understanding How DNA Repair Pathway Choice is Controlled
DNA double-strand breaks are the most toxic form of DNA damage and must be properly repaired to avoid cell death and cancer. This is highlighted by rare human genetic disorders such as ataxia-telangiectasia and Bloom syndrome, which are caused by mutations in genes involved in DNA double-strand break repair and predispose patients to cancer. Furthermore, some of the most effective cancer treatments work by inducing DNA double-strand breaks in tumour cells. Therefore, future study of DNA double-strand break repair is highly likely to lead to more effective cancer therapies in future.
It is still unclear how cells regulate the DNA double-strand break repair process. This project aims to shed light on this issue by studying how key DNA double-strand break repair proteins are controlled by protein-protein interactions and post-translational modifications, using advanced techniques in proteomics, super-resolution microscopy and CRISPR-Cas9 genome editing in human cells. In doing so, we will be attempting to answer a fundamental biological question in a clinically relevant area.