Characterising a novel mitochondrial damage control pathway and its importance in neurodegenerative disease

• PhD
• Honours

Mitochondrial dysfunction and inefficient mitochondrial damage control are implicated in neurodegenerative diseases including Parkinson’s Disease (PD). The goal of this project is to understand a new form of mitochondrial damage control that may be a new target for the treatment of PD. Interestingly, this novel pathway occurs independently of the best understood mitochondrial damage control pathway, regulated by the two ubiquitin enzymes PINK1 and Parkin, which are mutated in early onset PD.

Students will utilise cutting edge imaging techniques coupled with gene editing approaches to understand the key mechanisms of this novel pathway. Students will learn necessary skills to generate mammalian cell lines lacking genes of interest and express fluorescently tagged proteins. Students will receive training in biochemistry, cell biology, and will develop specific expertise in studying mitochondrial biology and inflammation in the brain. Completion of 3rd year biochemistry subjects is strongly recommended/desired.

Our labs’ (Lazarou, Dewson, and Lechtenberg) research is focused on the powerhouses of cells, structures called mitochondria, and the role of ubiquitin ligase machineries. Maintaining the integrity and function of mitochondria is essential for cells to survive and to grow, and the ubiquitin system plays a key role in this. Mitochondria are also central to the process of cell death termed apoptosis.

Defective function and integrity of mitochondria can lead to many diseases including Parkinson’s disease and cancer. Our research uses innovative approaches to better understand how cells in our body maintain their mitochondria to promote cell survival. This information is informing the development of new ways to treat a broad range of diseases with a specific focus on Parkinson’s disease.