Professor John Bateman
Professor John Bateman obtained his PhD in Biochemistry at Monash University and conducted postdoctoral research as a Fogarty Fellow at the National Cancer Institute (USA) studying gene regulation. On returning to The Royal Children's Hospital he initiated studies on the molecular basis of connective tissue diseases and is recognised internationally for his research into the molecular mechanisms of cartilage and bone development and inherited human disease.
He is a National Health and Medical Research Council (NHMRC) Senior Principal Research and Professorial Fellow in the Department of Biochemistry and Molecular Biology, University of Melbourne. He is a past president of the International Society for Matrix Biology and has served on the editorial boards of several major journals including The Journal of Biological Chemistry, The Biochemical Journal and Matrix Biology.
- Group Leader, Skeletal Biology and Disease, Murdoch Childrens Research Institute
- NHMRC Senior Principal Research Fellow, Murdoch Childrens Research Institute
1988: Research Fellow, NHMRC
1990: Senior Research Fellow, NHMRC
1990: Andre Lichwitz Prize - Institut National de la Sante et de la Recherche Medicale (INSERM), France
1996: Principal Research Fellow, NHMRC
2000- ongoing: Senior Principal Research Fellow, NHMRC
2005: Leverhulme Fellowship, University of Manchester, UK
2008: Barry Preston Award for distinguished contributions to extracellular matrix research - Matrix Biology Society of Australia and New Zealand
2009-2013: National Health and Medical Research Council Assignors Academy
In Australia, diseases of the musculoskeletal system are the second most prevalent medical conditions and a leading cause of health care expenditure with immense social impact. Professor Bateman's research program is directed at three interrelated aspects of musculoskeletal disease. Firstly, the molecular causes of inherited disorders of bone (such as osteogenesis imperfecta) and cartilage (chondrodysplasias), a large and diverse group of disorders. This research involves characterisation of new human disease genes and novel musculoskeletal disease mouse models.
A major focus of the research is to understand the functional consequences of the mutations – the molecular mechanisms of how the mutations cause disease. In this area a particular focus is the role of endoplasmic reticulum stress (unfolded protein response) that results from mutations that cause misfolding of secreted extracellular matrix proteins. This finding offers a new way of understanding disease mechanisms and opens up therapeutic possibilities.
A second major strand of Professor Bateman's research program explores another significant national health problem, osteoarthritis. His studies on the mechanisms of cartilage destruction in osteoarthritis are being used to identify disease candidates and biomarkers. These candidate genes/microRNAs are then studied in detail. Studies on the role of these genes in cartilage degenerative disease (and also in inherited disorders) are complemented by a third strand of the research program, the developmental biology of cartilage.
- The cell biology of protein misfolding (ER stress) in genetic cartilage and bone disease
- The use of induced pluripotential stem cells (iPSC) for functional genomic analysis of human genetic disease
- Understanding the molecular basis of brittle bone disease
- microRNAs in arthritis
- RNA surveillance – nonsense-mediated mRNA decay
Bateman, J.F., Boot-Handford, R.P. and Lamandé, S.R. (2009) Genetic diseases of connective tissues: Cellular and extracellular effects of ECM mutations Nature Reviews Genetics. 10(3):173-83 PMID: 19204719
Rajpar, M.H, McDermott, B., Eardley, R., Thornton, D.J., Wilson, R., Bateman, J.F., Poulsom, R., Arvan, P., Kadler, K.E., Briggs, M.D. and Boot-Handford R.P. (Targeted Induction of Endoplasmic Reticulum Stress Induces Cartilage Pathology. PLoS Genetics Oct; 5(10):e1000691 PMID: 19834559
Tsang, K.Y., Chan, D., Bateman, J.F. and Cheah K.S.E. (2010) In vivo cellular adaptation to ER stress: double edged survival strategies. J. Cell Science. Jul 1; 123(Pt 13):2145-54. PMID: 20554893
Wilson, R., Diseberg, A., Gordon, L., Zivkovic, S., Tatarczuch, L., Mackie, E., Gorman, J.J. and Bateman, J.F. (2010) Comprehensive profiling of cartilage extracellular matrix formation and maturation using sequential extraction and label-free quantitative proteomics. Molecular and Cellular Proteomics. Jun; 9(6): 1296-313. PMID: 20190199
Cameron, T.L., Bell, K.M., Tatarczuch ,L., Mackie ,E.J., Rajpar, M.H., McDermott, B.T., Boot-Handford ,R.P, and Bateman, J.F. (2011) Transcriptional Profiling of Chondrodysplasia Growth Plate Cartilage Reveals Adaptive ER-Stress Networks that Allow Survival but Disrupt Hypertrophy. PLoS One, 6(9):e24600. PMID: 21935428
Lamandé SR, Yuan Y, Gresshoff IL, Rowley L, Belluoccio D, Kaluarachchi K, Little CB, Botzenhart E, Zerres K, Amor DJ, Cole WG, Savarirayan R, McIntyre P, Bateman JF. (2011) Mutations in TRPV4 cause an inherited arthropathy of hands and feet. Nature Genetics. 2011 Oct 2;43(11):1142-6. doi: 10.1038/ng.945. PMID: 21964574
Wilson, R., Norris, E., Brachvogel, B., Angelucci, C., Zivkovic, S., Sterman, J., Sekiguchi, K., Gorman, J.J. and Bateman, J.F. (2012) Changes in the chondrocyte and extracellular matrix proteome during post-natal mouse cartilage development. Molecular and Cellular Proteomics. Jan;11(1):M111.014159. PMID: 21989018
Bateman, J.F., Rowley, L., Belluoccio, D., Chan, B., Bell, K ., Fosang, A.J. and Little, C.B. (2013) Transcriptomics of wild-typemice and mice lacking ADAMTS-5 activity identifies genes involved inosteoarthritis initiation and cartilage destruction. Arthritis and Rheumatism. Jun;65(6):1547-60. PMID: 23436205
Prockop, D.J. and Bateman J.F. (2012) Heritable disorders of connective tissue Harrison's Principles of Internal Medicine. 18th Edition. McGraw-Hill, New York. Chapter 363, p3204-3214.
Gossan, N., Zeef, L., Hensman, J., Hughes, A., Bateman, J.F., Rowley, L., Little, C.B., Rattray, M., Boot-Handford, R.P. and Meng, Q-J. (2013) The circadian clock in chondrocytes controls key aspects of cartilage homeostasis. Arthritis and Rheumatism. Sep;65(9):2334-45 PMID 23896777