Principal Advisor: Dr Mathew Jones


Organisational unit: UQ Diamantina Institute

DNA replication is the fundamental mechanism of genetic inheritance and an essential process for all cellular life. In cancer cells, replication is corrupted and replication forks frequently stall and collapse causing DNA damage and copying errors that drive tumorigenesis. As a result, cancer cells are heavily dependent on the pathways that protect and repair stalled replication forks. Disrupting these mechanisms can be selectively toxic to cancer cells. A key player in the regulation of DNA replication and repair is DDK (Dbf4-dependent kinase also known as Cdc7). DDK is frequently overexpressed in cancer, but its role during DNA replication and the repair of stalled replication forks has not been well characterised. Our research uses chemical genetic approaches to selectively target DDK and gain valuable insights into its requirements and molecular targets. This project aims to understand how DDK coordinates DNA replication and repair to help develop new therapeutic strategies to target these processes in cancer cells. This project is suitable for a PhD student and provides an excellent opportunity to learn molecular and cell biology techniques and gain experience with long-read genome sequencing tools and genome engineering methods (CRISPR/Cas9). A PhD scholarship is available for this project.