Two proteins, PINK1 and parkin, keep cells healthy by breaking down damaged mitochondria, cell's energy generators. This process is known as mitophagy or mitochondrial self-eating. Mutations -- genetic changes -- in PRKN and PINK1 disrupt this process and cause Parkinson's disease (PD). We have developed not only a detailed understanding of these proteins' functions but also methods -- genetic screens -- of identifying other genes that may control mitochondrial self-eating.
We propose using genetic screens to discover additional genes that control mitochondrial self-eating.
Using a newly developed experimental setup for studying mitochondrial self-eating, we will identify new candidate genes that control mitochondrial self-eating and confirm their role using conventional in vitro experimental setups.
Impact on Diagnosis/Treatment of Parkinson's disease:
Our current understanding of mitochondrial self-eating is limited. Identifying the genes involved in this process will allow researchers to conduct a more focused search for therapeutic molecules that may be able to correct defects of mitochondrial self-eating in people with PD.
Next Steps for Development:
Future studies would aim to discover small molecules able to correct deficiencies of mitochondrial self-eating identified through the genetic studies described here.