Dr Simon Myers

• Qualifications
• Biography
• Research
• Selected Publications
• Grants/currrent projects
• Teaching Interest
• Awards/Honours
• Professional Activities

Qualifications

BSc/DipEd; BSc-Hons I; PhD

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Biography

Dr. Simon Myers completed his PhD in molecular cell biology at the Heart Research Institute in Sydney, where he investigated altered protein expression and activation during atherosclerosis. He then completed a postdoctoral fellow position in molecular virology and host defence in the Department of Pathology at the University of Sydney (USyd) before moving to Apollo Life Sciences as Team Leader, Senior Research Scientist of Cell Biology program. Simon then moved back into medical research by taking up a Senior Research Fellow position at the ANZAC Research Institute, where he led the Cell Biology Program in the Northcott Neuroscience Laboratory. In 2008 Simon was successful in gaining a senior lectureship in Biochemistry at the University of Western Sydney (UWS).

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Research

Dr. Simon Myers's research investigates how mutations in house-keeping proteins alter normal cellular function of neuronal cells to cause neurodegenerative diseases and to identify common mechanisms between these diseases. Simon continues this research at the University of Western Sydney (UWS).

Axonal degeneration is the final common path in many neurological disorders. It is seen in its pure form in hereditary axonal neuropathies. The hereditary neuropathies are the most common group of diseases presenting to genetic counselling clinics with a prevalence of approximately 1 in 2500 population, thus affecting 8000 Australians.
 
Although they are rarely fatal they cause lifelong disability and thus have significant economic impact, estimated to be $180M per annum in Australia. No specific treatment is yet available for distal axonal neuropathies. These hereditary neuropathies with distal axonal degeneration are known as axonal Charcot-Marie-Tooth type 2 neuropathy (CMT2).

Nearly all hereditary neuropathies produce disability through the common feature of axonal degeneration. Even initial demyelinating forms of neuropathy eventually result in axonal degeneration. This is thought to be the result of disturbed Schwann cell and axonal interactions and possibly the spread of sodium channels. Although much is known about the cell biology of many of the neuropathy genes, little is known about how they produce axonal degeneration. CMT2A, HSN1 and DI-CMT1B are distal 'dying back' neuropathies which first affect the ends of motor and sensory nerves. Dying back has long been thought to be a result of an axonal transport problem.

Mutations were been identified in the dynamin 2 (Dyn2) which cause dominant-intermediate Charcot-Marie-Tooth (DI-CMTB) syndrome, an autosomal hereditary neuropathy. We have shown in DI-CMTB patient lymphoblast cells that the mutant Dyn2 blocks receptor mediated endocytosis (in collaboration with Prof. P Robinson and Dr. C Malladi from the Children's Medical Research Institute). These patient cells also display an accumulation of multi-vesicular bodies (MVBs), multi-lamellal bodies (MLBs) along with altered mitochondrial morphology.

Mutations in the serine palmitoyltransferase long chain subunit 1 (SPTLC1) protein cause HSN1. Pilot studies over-expressing the mutant SPTLC1 gene in human neuronal cells showed altered localisation of the SPTLC1 and changes to the actin cytoskeleton (in collaboration with Prof. G Nicholson from the ANZAC Research Institute). We have also shown that the HSN patient lymphoblasts do not have blocked receptor-mediated endocytosis (in collaboration with Prof. P Robinson and Dr. C Malladi from the Children's Medical Research Institute). Further investigations will elucidate how these changes attribute to neuronal cell dysfunction in this neurodegenerative disease. Recent preliminary studies have indicated that mitochondria play a role in HSN1 this exciting new finding will be another strong focus area for our HSN1 projects (in collaboration with Prof. G Nicholson from the ANZAC Research Institute).

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Selected Publications

Myers, S.J., and Stanley, K.K. (1999). Src family kinase activation in glycosphingolipid-rich membrane domains of endothelial cells treated with oxidised low-density lipoprotein. Atherosclerosis. 143: 389-397. (IF 3.800)

Bartlett, A.L., Grewal, T., De Angelis, E., Myers, S., and Stanley, K.K. (2000). Role of the macrophage galatose lectin in the uptake of desialylated LDL. Atherosclerosis. 153: 219-230. (IF 3.800)

Martinic, G., Myers, S., and Stanley, K. (2001). Methodology for the determination of the rate of transcytosis in a rat model. Animal Technology. 52: 97-101. (IF Not Available)

Kok, C., Kennerson, M.L., Myers, S.J., and Nicholson, G.A. (2004). Transcript map of the candidate region for HSNI with cough and GER on chromosome 3p and exclusion of candidate genes. Neurogenetics. 5: 197-200. (IF 2.938)

Rayner, B.S., Duong, T.T.H., Myers, S.J., and Witting, P.K. (2006). Protective effect of a synthetic antioxidant on neuronal cell apoptosis resulting from hypoxia re-oxygenation. J Neurochem. 97: 211-221. (IF 4.604)

Nicholson, G.A., and Myers, S.J. (2006). Intermediate forms of Charcot-Marie-Tooth neuropathy: a review. Neuromolecular Med. 8: 123-130. (IF 4.070)

Myers, S.J., Nicholson, G.A. (2006). Sphingolipid Biology: Hereditary Sensory Neuropathy. Springer-Verlag Tokyo.

Duong, T.T.H., Ellis, N.A., Rayner, B.S., Myers, S.J., and Witting, P.K. (2008). Gene regulation and apoptosis in cultured human neuronal cells exposed to hypoxia re-oxygenation injury as a model for stroke. Brain Research. 1219: 8-18. (IF 2.8)

Myers, J., Malladi, C., Kennerson, L., Marshan, A., Robinson, P., and Nicholson, G.A. (2008). Receptor mediated endocytosis is blocked in D2-CMT EBV transformed lymphoblasts expressing mutant (K558E) dynamin II (Manuscript in preparation)

Myers, S.J., Malladi, C., Bautista, T., Huang, M.L., Boadle, R., Robinson, P., and Nicholson, G.A. (2008).  Mitochondrial structural abnormalities in hereditary sensory neuropathy type 1. (Manuscript re-submitted, BBA Mol. Basis Dis.). (IF 3.6)

Malladi, C.S., Myers, S.J., Boadle, R., North, K., Robinson, P.J., and Nicholson, G. (2008). Mutation K558E in PH domain of dynamin II causes muscle damage and abnormal mitochondrial accumulation in CMT patients (Manuscript in preparation)

Myers, S.J., Malladi, C., Parton, R., Nicholson, G.A., and Robinson, P. (2008).  Identification of ultrastructural changes to DI-CMTB lymphoblasts expressing the pleckstrin homology domain mutation of dynamin 2 (K558E). (Manuscript in preparation)

Grants/Current projects

Grants obtained prior to starting at UWS include:

• 2005-2008 Philip Bushell Foundation - Chief Investigator
• 2006-2008 USA-MDA - Co-Principle Investigator
• 2006-2008 NH&MRC Project Grant - Senior Researcher
• 2006-2007 USYD Large Equipment Grant - Investigator
• 2005-2008 Philip Bushell Foundation - Co-Investigator
• 2005-2006 NHMRC Equipment Grant - Investigator
• 2003 NHMRC Equipment Grant - Investigator

Since commencing at UWS:

• 2009 UWS-RIF Equipment Grant - Chief Investigator
• 2009 UWS-SBHS, Research Grant - Chief Investigator
• 2009 UWS-SBHS, Research Grant - Co-Chief Investigator
• 2009-2011 NHMRC Project Grant - Associate Investigator
• 2008-2011 Philip Bushell Foundation - Chief Investigator
• 2008 UWS-SBHS, Research Grant - Chief Investigator
• 2008 UWS-SBHS, Research Grant - Co-Chief Investigator
• 2008 UWS-CHS, Research Grant - Co-Chief Investigator
• 2008 RIF Equipment Grant - Co-Investigator

Current Projects 

1. Determining whether changes in electrophysiological signalling are present in neuronal cells expressing neurodegenerative disease causing mutants of SPTLC1C
2. Consequences of serine palmitoyltransferase long chain subunit 1 mutations on protein and lipid profiles in neuronal cells
3. Determining the common cellular and molecular mechanisms by which the mutant 'house-keeping like' proteins (Dynamin 2 and Serine palmitoyltransferase) cause sensory neuropathies
4. Determining cytoskeletal changes to cellular architecture due to PH domain dynamin 2 mutations
5. Do mutations in serine palmitoyltransferase long chain sub unit 1 affect the neuronal cell cytoskeleton

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Teaching Interests

Simon's teaching interests lie in Protein and Metabolic Biochemistry, and Molecular and cellular Immunology. Simon is the Unit Coordinator for Protein and Genes, Human Metabolism and Disease, Molecular Biology of the Immune System and lectures into Biomeolcular Frontiers unit.

Awards/Honours

• 2005: Winner of the University of Sydney's Vice-Chancellor's Award for Support of the Student Experience (in recognition of an outstanding contribution to the student experience at the University of Sydney)
• 1996: Winner of the AMRAD Pharmaceuticals Young Investigator Award for research presented at the Australian Atherosclerosis Society Meeting
• 1996: Recipient of the following travel grant awards 'AMRAD Pharmacia Biotech and Australian Atherosclerosis Society Trust Fund'
• 1994: Recipient of the following travel grant awards 'Sydney University and Australian Atherosclerosis Society Trust Fund'
• 1994-1997: Australian Postgraduate Award
• 1994-1997: Postgraduate Award from Australian Atherosclerosis Society Trust Fund for consumable support for the HRI
• 1994: Channel 10 Young Achievers Award - Top 10 Science and Technology category (special recognition)
• 1994: Finalist - The Thompson Prize, Sydney Protein Group.  'Characterization of altered protein expression in modified LDL loaded mouse peritoneal macrophages'

Professional Activities

• Executive Member and Theme Leader, Neurobiology of the UWS Molecular Medicine Research Group
• Executive Member of the School of Biomedical and Health Sciences Academic Committee
• Member of School of Biomedical and Health Sciences (SBHS) Academic Committee
• SBHS Learning and Teaching Fellow
• Conjoint Senior Lecturer in School of Medicine, UWS
• Conjoint Senior Research Fellow Concord Clinical School, Faculty of Medicine, University of Sydney