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Monash University > Medicine, Nursing and Health Sciences > Department of Biochemistry and Molecular Biology > Staff >

Professor Phillip Nagley

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Professor Phillip Nagley

BSc (Hons), MSc (University of Sydney), PhD, DSc (Monash University)

Phillip Nagley

Telephone : +61 3 9905 3735
Facsimile:    +61 3 9902 9500
Office:            Room G31, Building 77
Email:             phillip.nagley@monash.edu 

General Profile:

  • I am a Professor of Biochemistry, with enthusiasm for all aspects of Biochemistry and Molecular Biology.
  • My particular research interests encompass mitochondria, oxidative stress and the variety of cell death patterns, particularly in neuronal cells.
  • I am Director of Education in the School of Biomedical Sciences.
  • I was editor (1998 - 2003) of the Australian Biochemist, the national scientific and news magazine of the Australian Society for Biochemistry and Molecular Biology.
  • I was President-elect of ASBMB (2004), President of ASBMB (2005-2006), Past-president (2007).
  • I am Secretary General of the Federation of Asian and Oceanian Biochemists and Molecular Biologists (FAOBMB) from 2012.
  • I was awarded the Lemberg Medal of the Australian Society for Biochemistry and Molecular Biology in 2001.
  • I was awarded the Dean's Award for Excellence in Research, Faculty of Medicine, Nursing and Health Sciences in 2003.
  • I was co-chair of the OzBio2010 Conference (12th IUBMB-21st FAOBMB-ComBio2010 combined Conference) held in Melbourne, September 2010.
  • I was Convenor of the Young Scientist Forum (YSF), held in association with OzBio2010, in which early career researchers from all over the world and Australia participated.

Current Research Interests:

  • Mitochondria and oxidative stress in neuronal injury and cell death 
  • Significance of mitochondria in survival and death of cancer cells
  • The process of release of apoptotic signalling proteins from mitochondria
  • Understanding host-pathogen interactions in bacterial infection of mammalian cells

Career Synopsis and Research Profile

Professor Phillip Nagley graduated from the University of Sydney in 1967, where he was awarded the University Medal in Biochemistry. He completed his MSc at the same University before moving to Melbourne to undertake his PhD in the Department of Biochemistry at Monash University. His research work at Sydney encompassed studies of mammalian ribosomes and endoplasmic reticulum, then work on bacterial DNA replication. He integrated these two different experiences to embark on his PhD studies on the formation of mitochondria in yeast cells.

Phillip Nagley's PhD studies, completed in 1972, focussed on a molecular genetic and biochemical study of mitochondrial biogenesis. One highlight of this early work was the discovery he made of yeast cells that lack mitochondrial DNA (mtDNA) completely. These cells were termed rho0 by Nagley and Linnane (1972), a term which is current use today for similar cells that can be isolated from mammalian sources and which are extremely useful in many aspects of research on the role of mitochondria in cellular life and death.

Phillip Nagley continued his research in the Department of Biochemistry (now Biochemistry and Molecular Biology) at Monash University since 1972, with two periods of sabbatical leave at the University of Paris, France, and Stanford University, California, USA. He has also held Exchange Fellowships for collaboration with scientists in Japan (University of Nagoya, University of Tokushima) and Taiwan (National Yang-Ming University).

He has researched extensively into the formation of mitochondria in yeast, covering many aspects of cell and molecular biology. He was awarded his DSc degree in 1986 for his collected publications to that time, in a thesis entitled The Molecular Biology of Mitochondria. He was awarded a Personal Chair in Biochemistry in 1990. He has published more than 200 publications in international journals and books.

Most of Professor Nagley's research up to 1990 was on the yeast system. A seminal innovation made in the 1980s was the development of "allotopic expression" (Nagley and Devenish, 1989). This procedure involves restoration of function in mitochondria damaged by mitochondrial genetic defects. The process of allotopic expression occurs through expression of relevant genes in the nucleus and targeting the restorative molecules back to mitochondria. It is pursued by many laboratories worldwide in the context of mitochondrial disease and ageing.

His work since then has moved to mammalian systems, including ageing, cell death pathways and cellular response to oxidative stress. Most recently his work includes detailed studies on the role of mitochondria in cell death, particularly in neuronal systems where the diversity of cell death responses is being clarified.

Highlights of this recent work are encompassed by the following reviews:

D.J. Smith, H. Ng, R.M. Kluck and P. Nagley. "The mitochondrial gateway to cell death". IUBMB Life, 60, 383-389 (2008)

P. Nagley, G.C. Higgins, J.D. Atkin and P.M. Beart. "Diverse deaths orchestrated by mitochondria in neuronal systems". Biochimica et Biophysica Acta - Molecular Basis of Disease, 1802, 167-185 (2010)

G.C. Higgins, P. M. Beart, Y. S. Shin, M. J. Chen, N. S. Cheung and P. Nagley. "Oxidative Stress: Emerging mitochondrial and cellular themes and variations in neuronal injury". Journal of Alzheimer's Disease, 20, Suppl. 2, S453-S473 (2010)

Some primary research publications in this area (amongst many others) are as follows:

K.Y. Soo, J.D. Atkin, M.K. Horne and P. Nagley. "Recruitment of mitochondria into apoptotic signalling correlates with the presence of inclusions formed by amyotrophic lateral sclerosis-associated SOD1 mutations". Journal of Neurochemistry, 108, 578-590 (2009)

G.C. Higgins, P.M. Beart and P. Nagley. "Oxidative stress triggers neuronal caspase-independent death: Endonuclease G involvement in Programmed Cell Death-Type III". Cellular and Molecular Life Sciences, 66, 2773-2787 (2009)

G.C. Higgins, R. J. Devenish, P. M. Beart and P. Nagley. "Autophagic activity in cortical neurons under acute oxidative stress directly contributes to cell death". Cellular and Molecular Life Sciences, 68, 3725-3740 (2011)

K.Y. Soo, J.D. Atkin, M. Farg, A.K. Walker, M.K. Horne and P. Nagley. "Bim links ER stress and apoptosis in cells expressing mutant SOD1 associated with amyotrophic lateral sclerosis". PLoS ONE, 7, e35413 (2012)

 

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