Major Areas of Research
- Prion diseases
- Prion redox biology
- Prion protein processing and function
The Prion Cell Biology Unit is focused on elucidating the underlying cellular pathways causing neuronal death and dysfunction during prion diseases, as well as understanding the basic cellular functions of the prion protein. We have a specific interest in the role of the prion protein in cellular redox homeostasis and how perturbations in redox balance influence disease progression and toxicity. The unit is utilizing and developing new stem cell-based models of prion infection, which will be used to investigate cell type and region-specific reactions to prion strains together with how complex multi-cell-type cultures respond as infection develops over time.
Dr. Haigh received her Ph.D. in Biochemistry from the University of Bath (UK) in 2006. Her thesis focused on the cellular function of the prion protein and genetic control of its expression.
In July 2006, she relocated to The University of Melbourne (Australia) to continue working on the cellular function and post-translational modifications of the prion protein as a post-doctoral fellow. Following securing further Australian funding, Dr. Haigh’s research branched into several new areas; redox imbalance throughout the course of prion infection, the development of stem cell models of prion disease and the role of the prion protein in controlling stem cell functions.
In 2017, Dr. Haigh accepted a tenure track position at the Rocky Mountain Laboratories to further her research into redox homeostasis and prion biology. She currently serves on the editorial board of Cell Biochemistry and Biophysics.
Collins SJ, Haigh CL. Simplified Murine 3D Neuronal Cultures for Investigating Neuronal Activity and Neurodegeneration. Cell Biochem Biophys. 2017 Mar;75(1):3-13. doi: 10.1007/s12013-016-0768-z.
Collins SJ, Tumpach C, Li QX, Lewis V, Ryan TM, Roberts B, Drew SC, Lawson VA, Haigh CL. The prion protein regulates beta-amyloid-mediated self-renewal of neural stem cells in vitro. Stem Cell Res Ther. 2015 Apr 11;6:60. doi: 10.1186/s13287-015-0067-4.
Haigh CL, Tumpach C, Drew SC, Collins SJ. The Prion Protein N1 and N2 Cleavage Fragments Bind to Phosphatidylserine and Phosphatidic Acid; Relevance to Stress-Protection Responses. PLoS One. 2015 Aug 7;10(8):e0134680.
Haigh CL, McGlade AR, Collins SJ. MEK1 transduces the prion protein N2 fragment antioxidant effects. Cell Mol Life Sci. 2015 Apr;72(8):1613-29. doi: 10.1007/s00018-014-1777-y.
Le Brun AP, Haigh CL, Drew SC, James M, Boland MP, Collins SJ. Neutron reflectometry studies define prion protein N-terminal peptide membrane binding. Biophys J. 2014 Nov 18;107(10):2313-24. doi: 10.1016/j.bpj.2014.09.027.
Sinclair L, Lewis V, Collins SJ, Haigh CL. Cytosolic caspases mediate mislocalised SOD2 depletion in an in vitro model of chronic prion infection. Dis Model Mech. 2013 Jul;6(4):952-63. doi: 10.1242/dmm.010678.