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Function correlation in CtIP: a key DNA repair factor implicated in human disease


School of Biochemistry

Bristol United Kingdom Biochemistry

About the Project

The repair of double‐stranded DNA breaks (DSBs) is central to many aspects of cell biology, human disease and biotechnology. In healthy cells, DSBs must be repaired frequently as the result of inevitable DNA damage and replication fork collapse, but they are also generated deliberately to promote desirable genetic re‐arrangements. In the disease state, failure to correctly repair DSBs acts as a primary driver of genetic instability and cancer. Nevertheless, the induction of DSBs is central to the mechanism of action of chemotherapeutic agents, anti‐microbials and CRISPR‐Cas gene‐editing technology. The long‐term aim of work in the Dillingham laboratory is to bring mechanistic clarity to our understanding of double‐stranded DNA break repair in human cells to underpin each of these important fields.

In this PhD project, you will study the human DNA repair factor CtIP; an enigmatic protein playing an important role in the regulation of the resectosome which initiates the recombinational repair of double-stranded DNA breaks. It acts as a hub to integrate signalling cues and co‐ordinates the broken DNA with activity and recruitment of many other repair factors. Despite intense interest from both a
basic science and human disease perspective, we still have an exceptionally poor understanding of CtIP at the molecular level. The proposed PhD project will remedy this by building directly upon our recent breakthrough work.

Using an interdisciplinary combination of biochemical, biophysical and cell biological approaches you will study the interactions between CtIP, its partner proteins and broken DNA in order to provide new mechanistic insights into DSB repair regulation and the molecular basis for human disease including cancer.

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