Abstract

Ageing and age-related diseases such as cancer are characterised by the dysregulation of cell growth pathways. In healthy cells, growth is controlled by the dynamic balance between biosynthesis, degradation and recycling mediated, in part by the mTORC1-autophagy pathway. Cellular stress such as oncogene activation and DNA damage can cause senescence or transformation which are associated with a comprehensive rewiring and re-equilibrium between these processes. I will be presenting data detailing how mTORC1 activity becomes insensitive to nutrient withdrawal in senescent and melanoma cells which is mediated by gross changes in the autophagy-lysosome pathway. Ultimately, I am interested in understanding the mechanisms that enable cells to adapt and harness catabolic processes to support growth and survival.