The Ganley lab is interested in unravelling the molecular mechanism of autophagy (which literally translates from the Greek meaning to eat oneself). Autophagy 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. The autophagy field is a rapidly growing area of research, one of the reasons being that it is dysregulated in many diseases and therefore its modulation could lead to novel therapies. 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 (Allen et al., EMBO Rep, 2013; McWilliams et al., J Cell Biol, 2016), 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..
We offer a 4 year studentship in which you would join a particular lab in the Unit. However, we strongly encourage prospective students to become part of the 4-year PhD programme in which you carry out rotation projects in two labs within the Unit (http://www.ppu.mrc.ac.uk/studentships/phd_projects.php). This studentship is jointly funded by the Medical Research Council and the University of Dundee and carries a tax-free stipend of £20,000 per annum
Allen, G. F., Toth, R., James, J. and Ganley, I. G. (2013). Loss of iron triggers PINK1/Parkin-independent mitophagy. EMBO Rep 14, pp. 1127-1135
McWilliams, T. G., Prescott, A. R., Allen, G. F., Tamjar, J., Munson, M. J., Thomson, C., Muqit, M. M. and Ganley, I. G (2016). mito-QC illuminates mitophagy and mitochondrial architecture in vivo. J Cell Biol 214, pp. 333-345