Investigating the role of dysregulated Tom40 in neurodegeneration

Investigating the role of dysregulated Tom40 in neurodegeneration

Project details

Age-related neurodegenerative diseases are associated with changes in mitochondrial function leading to cell death. A strong genetic association between Alzheimer’s disease and altered Tom40 expression (caused by gene polymorphisms) has been noted. 

We have recently established that altered expression of Tom40, a key component of a translocase associated with mitochondrial biogenesis (TOM), invokes caspase-dependent cell death and neurodegeneration that is contingent upon the availability of other TOM components, implicating the translocase.  

Available projects are based on using structural, imaging and/or genetic methods to investigate the changes in TOM assemblies, protein interactions and localisation that are invoked in death and neurodegeneration pathways. 

The primary location is in the Structural Biology division, but projects are collaborative with other labs at WEHI and elsewhere. 

About our research group

Our interests are in gaining an understanding of the complex allosteric mechanisms controlling potassium channels with a view to unlocking their therapeutic potential, to date an elusive goal for drug companies. We are also interested in mitochondrial translocases and have applied genetic methods to investigate association of translocase subunits with proteins from the apoptotic quality control in tissues undergoing Tom40-induced cell death  (with particularly relevance to this project). We use structural (X-ray crystallography, Cryo-EM), biochemical, and biophysical methods to interrogate mechanism.  

Key collaborations for this project: 

Associate Professor Leonie Quinn (JCSMR, ANU) 

Dr Kelly Rogers (WEHI Centre for Dynamic Imaging) 

Professor Dr Werner Kühlbrandt (MPI, Frankfurt) 


Email supervisors



Dr Jacqui Gulbis

Dr Jacqui Gulbis
Laboratory Head
Dr Agalya Periasamy
Structural Biology division

Project Type: