Dr Ian Ganley

Scientific Programme Leader (MRC)

MRC PPU, School of Life Sciences

Portrait photo of Ian Ganley
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Contact

Email

i.ganley@dundee.ac.uk

Phone

+44 (0)1382 388905

Locations

James Black Centre

Websites

Ganley Lab

Research

We are interested in a cell protective mechanism termed autophagy.

The cells of our body are constantly exposed to potentially damaging agents from both external sources, such as the sun's harmful UV rays or pathogenic bacteria, as well as internal sources, including free radicals produced by the cells metabolic pathways. Thankfully we have multiple mechanisms to help us cope with this onslaught. One such protection mechanism is autophagy (which literally means self-eating), whereby damaged and unwanted cellular components are targeted for degradation and recycling. These components are engulfed by a specialised structure known as the autophagosome and delivered to the digestive lysosome. This essential process prevents the cell from ending up a rubbish dump, and because of this, impaired autophagy has been linked to many diseases.

What are the signals that initiate autophagy?

We want to decipher the phosphorylation and ubiquitylation events that switch on autophagy and determine how these pathways target specific cellular components. A large part of our work focusses on two autophagy-essential kinase complexes containing either the protein kinase ULK1 or the lipid kinase VPS34. It is thought that both kinase complexes play an important role in non-specific autophagy (the random targeting of subcellular components) as well as specific autophagy. We are trying to determine how these complexes are turned on or off and if they perform the same function in specific vs. non-specific autophagy

See figure 1 below

Can autophagy be targeted to treat disease?

To aid in studying how specific components are targeted, we have developed a simple and robust assay to monitor mitophagy, the specific autophagy of mitochondria. Dysfunctional mitophagy has been linked to many diseases including cancer, Parkinson’s and heart disease. With the aid of our assay, we have uncovered mitophagy-inducing pathways and are now characterising how the interplay between phosphorylation and ubiquitylation activates the autophagy machinery to drive mitochondrial degradation. It is our hope that modulation of these identified pathways will have therapeutic value.

See figure 2 below

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Stories

Research interests

Molecular analysis of autophagy