Regulation of stress responses in ageing and disease

Ageing occurs by the accumulation of damage to cells leading to progressive deterioration of physiological functions. It is influenced by both genetic and environmental factors. Importantly, genetic manipulations that slow ageing can also delay the onset of many diseases such as cancer and those associated with neuronal and muscle degeneration. Therefore, targeting the molecular basis of ageing may also protect from ageing-related disease. The signalling pathways that regulate lifespan are often associated with the cellular response to stress or nutrients. Mitochondrial function is sensitive to both and mutations in a number of genes encoding mitochondrial proteins affect lifespan. Mitochondria are a major source of reactive oxygen species (ROS) that are by-products of the electron transport chain. ROS can cause damage to cells so it is important for mitochondria to communicate effectively with the nucleus to promote protective responses and maintain homeostasis. Projects are available to investigate how signals from mitochondria regulate transcriptional responses and how these contribute to ageing and ageing-related disease.

Approaches used will include mammalian cell culture, C. elegans transgenics, recombinant protein expression, mutagenesis, qPCR, immunoblotting and immunoprecipitation, fluorescence microscopy, RNAi, CRISPR gene editing and genomics.

Candidates are expected to hold (or be about to obtain) a minimum upper second class honours degree (or equivalent) in a related area / subject.