Dr Amanda Coutts – Senior Lecturer in Molecular Biosciences and Group Leader: Cancer cell survival and stress response.

After obtaining a PhD in Molecular Biology and Biochemistry (University of Manitoba), Amanda undertook postdoctoral studies at the Beatson Institute for Cancer Research, University of Glasgow, Dept of Biochemistry, and the University of Oxford, Dept of Oncology, before joining Nottingham Trent University as a Senior Lecturer. At NTU she established her first independent research group (John van Geest Cancer Research Centre (JvGCRC), SHiMR research Centre) where her research focuses on understanding how cancer cell survival pathways link to disease progression and how stress responses influence nuclear structure and function.

Mechanisms influencing cell survival such as apoptosis and autophagy are key determinants of cell fate during stress. Importantly, understanding how the cell integrates a variety of signals to affect a cellular outcome is clinically relevant and a poorly understood process. My 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, and particularly, the role of actin in these processes. During this seminar I will discuss some recent research that has uncovered novel links with splicing regulators and nuclear actin. While evidence supports an important functional role of nuclear actin in processes fundamental to gene expression and cellular phenotype, the molecular details and key players are underexplored. We have recently identified nuclear filamentous (F)-actin formation in response to specific modulators of pre-mRNA splicing. Moreover, this has uncovered links with nuclear F-actin and the nucleolar stress response – thus suggesting that under certain conditions the formation of nuclear F-actin triggers a unique stress response that impacts cancer cell survival. We hope to better understand how stress responses impact nuclear structure and function, how this influences cancer cell survival, ultimately aiming to leverage this to enable translational impacts.