After obtaining a PhD in Molecular Biology and Biochemistry, Dr Coutts undertook postdoctoral studies at the Beatson Institute for Cancer Research (1999-2004), the University of Glasgow (2004-2005), and the University of Oxford (2005-2016), before joining Nottingham Trent University in August 2016.

Cancer, p53 and its co-factor JMY, autophagy and cell survival

Tumour growth is achieved by overriding cell cycle control and bypassing cell death. Mechanisms influencing cell survival such as apoptosis and autophagy are key determinants of cell fate during stress. Moreover, during tumour progression the acquisition of metastatic potential is the most devastating event in human cancer with metastatic disease the cause of 90% of cancer deaths. Importantly, understanding how the cell integrates a variety of signals to affect a cellular outcome is clinically relevant and a poorly understood process.

Dr Coutt’s work involving the p53 co-factor JMY has uncovered novel links between cell motility and the DNA damage response as well as mechanisms involved in autophagy and cell survival. Her research seeks to explore how a transcription co-factor links the cytoskeleton with nuclear events during the stress response, how this impacts on p53 activity and cell survival, and the role of actin in these processes.

Opportunities to carry out postgraduate research towards an MPhil / PhD may exist and further

Actin nucleation and autophagosome formation. Coutts AS, La Thangue NB. Cellular and Molecular Life Sciences, 73:3249-63, 2016. Actin nucleation by WH2 domains at the autophagosome. Coutts AS and La Thangue NB. Nature Communications, 6: 2015. DOI: 10.1038/ncomms8888. Cofactor Strap regulates oxidative phosphorylation and mitochondrial p53 activity through ATP synthase. Maniam S*, Coutts AS*, Stratford MR, McGouran J, Kessler B, La Thangue NB. Cell Death and Differentiation, 22: 156-163, 2015. *joint 1st. Cancer Cell Death. Coutts AS, Maniam S, and La Thangue NB. Oxford Textbook of Oncology, Oxford University Press. 2015. E2F-7 couples DNA-damage dependent transcription with the DNA repair process. Zalmas LP, Coutts AS, Helleday T, La Thangue NB. Cell Cycle, 12:3037-3051, 2013. Hypoxia-driven cell motility reflects the interplay between JMY and HIF-1a. Coutts AS, Pires IM, Weston L, Buffa FM, Milani, M, Li J-L, Harris AL, Hammond EM and La Thangue NB. Oncogene, 30: 4835-4842, 2011. A transcription co-factor integrates cell adhesion and motility with the p53 response. Coutts AS, Weston L, and La Thangue NB. Proceedings of the National Academy of Sciences., 106: 19872-19877, 2009. p53-cofactor JMY is a multifunctional actin nucleator. Zuchero BJ, Coutts AS, Quinlan ME, La Thangue NB, and Mullins RB. Nature Cell Biology., 11: 451-459, 2009.