Dr Mathew Jones

Senior Lecturer

School of Chemistry and Molecular Biosciences
Faculty of Science

Senior Research Fellow

Frazer Institute
Faculty of Medicine
mathew.jones@uq.edu.au
+61 7 336 54878

Overview

Qualifications

  • Doctor of Philosophy, The University of Queensland

Publications

  • Nguyen‐Dien, Giang Thanh, Kozul, Keri‐Lyn, Cui, Yi, Townsend, Brendan, Kulkarni, Prajakta Gosavi, Ooi, Soo Siang, Marzio, Antonio, Carrodus, Nissa, Zuryn, Steven, Pagano, Michele, Parton, Robert G, Lazarou, Michael, Millard, S Sean, Taylor, Robert W, Collins, Brett M, Jones, Mathew JK and Pagan, Julia K (2023). FBXL4 suppresses mitophagy by restricting the accumulation of NIX and BNIP3 mitophagy receptors. The EMBO Journal, 42 (13) e112767, e112767. doi: 10.15252/embj.2022112767

  • Bonfim-Melo, Alexis, Noordstra, Ivar, Gupta, Shafali, Chan, Amy H., Jones, Mathew J.K., Schroder, Kate and Yap, Alpha S. (2022). Rapid lamellipodial responses by neighbor cells drive epithelial sealing in response to pyroptotic cell death. Cell Reports, 38 (5) 110316, 110316. doi: 10.1016/j.celrep.2022.110316

  • Rashidieh, Behnam, Molakarimi, Maryam, Mohseni, Ammar, Tria, Simon Manuel, Truong, Hein, Srihari, Sriganesh, Adams, Rachael C., Jones, Mathew, Duijf, Pascal H. G., Kalimutho, Murugan and Khanna, Kum Kum (2021). Targeting BRF2 in cancer using repurposed drugs. Cancers, 13 (15) 3778, 1-28. doi: 10.3390/cancers13153778

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Supervision

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Available Projects

  • 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).

View all Available Projects

Publications

Book Chapter

Journal Article

PhD and MPhil Supervision

Current Supervision

Completed Supervision

Possible Research Projects

Note for students: The possible research projects listed on this page may not be comprehensive or up to date. Always feel free to contact the staff for more information, and also with your own research ideas.

  • 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).