Dr Tom Wishart

The Roslin Institute

Research Interests

Research Summary: 

Research in the Wishart laboratory is aimed at understanding the cellular and molecular processes which underpin the development and stability of the nervous system in health and disease, with a more specific focus on the biology of the neuron.

It is accepted that the neuron can be compartmentalized (grossly speaking) with respect to both form and function into three units: the cell body (or soma and associated dendrites), the axon and the synapse. It is also known that stability of the axon and synapse can be affected independently of one another. 

Synapses are of special interest to us as it is becoming increasingly accepted that they are a primary pathological target in a number of neurodegenerative conditions, including but by no means limited to; Alzheimer’s disease, Parkinson’s disease, Huntington’s disease and motor neuron diseases. That is to say, synapses go first and the rest of the neuron follows. As age increases the susceptibility to many of these neurodegenerative conditions, the ever increasing life expectancy of current society means that the costs associated with neurodegenerative diseases are only going to escalate over the coming years. It is therefore critical that we develop a clearer understanding of the mechanisms which underpin healthy development and stability of synapses and the regulators of altered synaptic/neuronal vulnerability.

In order to address these points we combine anatomical knowledge with high resolution imaging and biochemical/molecular biological techniques in vivo and in vitro to identify the key players and tease apart the mechanisms involved in these processes.

 For further information please go to:
 
http://www.roslin.ed.ac.uk/tom-wishart/summary-of-research/

Selected Publications

  • Thomas M Wishart, Chantal A Mutsaers, Markus Riessland, Michell M Reimer, Gillian Hunter, Marie L Hannam, Samantha L Eaton, Heidi R Fuller, Sarah L Roche, Eilidh Somers, Robert Morse, Philip J Young, Douglas J Lamont, Matthias Hammerschmidt, Anagha Joshi, Peter Hohenstein, Glenn E Morris, Simon H Parson, Paul A Skehel, Thomas Becker, Iain M Robinson, Catherina G Becker, Brunhilde Wirth, Thomas H Gillingwater. 2014. Dysregulation of ubiquitin homeostasis and beta-catenin signaling promote spinal muscular atrophy. Journal of Clinical Investigation Vol: 124 Pages: 1821-1834. More»
  • Chantal A. Mutsaers, Douglas J. Lamont, Gillian Hunter, Thomas M. Wishart, Thomas H. Gillingwater. 2013. Label-free proteomics identifies Calreticulin and GRP75/Mortalin as peripherally accessible protein biomarkers for spinal muscular atrophy. Genome Medicine Vol: 5. More»
  • Samantha L. Eaton, Sarah L. Roche, Maica Llavero Hurtado, Karla Suchacki, Colin Farquharson, Thomas H. Gillingwater, Thomas M. Wishart. 2013. Total Protein Analysis as a Reliable Loading Control for Quantitative Fluorescent Western Blotting. PLoS One Vol: 8. More»
  • Thomas M Wishart, Timothy M Rooney, Douglas J Lamont, Ann K Wright, A Jennifer Morton, Mandy Jackson, Marc R Freeman, Thomas H Gillingwater. 2012. Combining Comparative Proteomics and Molecular Genetics Uncovers Regulators of Synaptic and Axonal Stability and Degeneration In Vivo. PLoS Genetics Vol: 8. More»
  • J. W. Benedict, A. L. Getty, T. M. Wishart, T. H. Gillingwater, D. A. Pearce. 2009. Protein Product of CLN6 Gene Responsible for Variant Late-Onset Infantile Neuronal Ceroid Lipofuscinosis Interacts with CRMP-2. Journal of Neuroscience Research Vol: 87 Pages: 2157-2166. More»
  • C. Kielar, T. M. Wishart, A. Palmer, S. Dihanich, A. M. Wong, S. L. Macauley, C. H. Chan, M. S. Sands, D. A. Pearce, J. D. Cooper, T. H. Gillingwater. 2009. Molecular correlates of axonal and synaptic pathology in mouse models of Batten disease. Human Molecular Genetics Vol: 18 Pages: 4066-4080. More»
  • T. M. Wishart, J. P. W. Huang, Lyndsay Murray, D. J. Lamont, C. A. Mutsaers, J. Ross, P. Geldsetzer, O. Ansorge, K. Talbot, S. H. Parson, T. H. Gillingwater. 2010. SMN deficiency disrupts brain development in a mouse model of severe spinal muscular atrophy. Human Molecular Genetics Vol: 19 Pages: 4216-4228. More»