The Ganley lab is interested in unravelling the molecular mechanism of autophagy (which literally translates from the Greek meaning to eat oneself). Autophagy is a lysosomal degradation pathway that functions to clear the cell of potentially damaging agents, such as protein aggregates or faulty mitochondria, as well as acting as a recycling station to supply essential building blocks during periods of starvation. Importantly, autophagy appears to be dysregulated in many diseases and therefore its modulation could lead to novel therapies. However, to enable this, we first need to understand the machinery involved. A project is available to decipher the signals that lead to the specific autophagy of mitochondria (termed mitophagy), a process that has been linked to Parkinson’s disease and cancer. Following up on recently published work (see McWilliams et al. Cell Metabolism, 2018 and Singh et al. eLife, 2021), the project will utilise state-of-the-art microscopy, protein biochemistry and high-throughput screening to identify phosphorylation and ubiquitylation events involved in capturing mitochondria for degradation.