Epigenetics and Mitochondrial Biology Lab


With life expectancies increasing around the world, neurodegenerative disorders (e.g. Alzheimer's disease -AD, Parkinson's disease - PD, Motor neuron diseases - MND) represent an enormous disease burden on individuals, families, and society. Two forms of cellular stress are associated with practically every single age-related neurodegenerative disease: mitochondrial dysfunction, and toxicity resulting from conformationally challenged, aggregate-prone proteins. Although direct links between these factors and human disease are sometimes elusive, it is clear that such stresses ultimately lead to a decline in individual neuron function over time.

The Zuryn lab uses cutting-edge molecular techniques in the highly successful genetic model organism C. elegans as well as human cell culture to understand the fundamental mechanisms that promote disease progression caused by mitochondrial dysfunction. Mitochondria harbour their own genome (mtDNA), which is prone to accumulating mutations as we age leading to dysfunction that may contribute to the progressive nature of neurodegenerative diseases. The Zuryn lab have recently discovered that certain cell types in the body are prone to propagating mtDNA mutations (Ahier et al. Nature Cell Biology 2018) and that aggregate-prone disease-associated proteins can enhance the accumulation of mtDNA mutations in neurons by inhibiting quality control pathways, such as mitophagy (Cummins et al. EMBO Journal 2019, Ahier et al BioRxiv 2020). Excitingly, the Zuryn lab are now uncovering mechanisms that counteract the mtDNA mutations themselves by developing novel genetic tools that allow them to probe cellular responses and protective mechanisms that reverse the effects of mtDNA damage. Their aim is to discover new molecules that protect cells from the effects of mitochondria dysfunction and that can then be used as potential therapeutic targets to counteract mitochondrial and neurodegenerative disease.



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Group Publications

Research Areas

  • Mitochondrial Biology
  • Epigenetics
  • Neurodegeneration
  • Mitochondrial diseases


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Research Members



Ahier et al 2018. Front cover.

Ahier A, Dai CY, Tweedie A, Bezawork-Geleta A, Kirmes I, Zuryn S. (2018). Affinity purification of cell-specific mitochondria from whole animals resolves patterns of genetic mosaicism. Nature Cell Biology. 20(3):352-360.

Hahn A & Zuryn S (2018). The cellular mitochondrial genome landscape in disease. Trends in Cell Biology. (in press).

Cummins N, Tweedie A, Zuryn S, Bertran-Gonzalez J, Götz J (2018) Disease-associated tau impairs mitophagy by inhibiting Parkin translocation to mitochondria. EMBO Journal (In Press).

Bezawork-Geleta A, Wen H, Dong L, Bing Y, Vider J, Boukalova S, Krobova L, Vanova K, Zobalova R, Sobol M, Hozak P, Novais SM, Caisova V, Abaffy P, Naraine R, Pang Y, Zaw T, Zhang P, Sindelka R, Kubista M, Zuryn S, Molloy MP, Berridge MV, Pacak K, Rohlena J, Park S, Neuzil J (2018). Alternative assembly of respiratory complex II connects energy stress to metabolic checkpoints. Nature Communications. 9:2221.

Zuryn S, Ahier A, Portoso M, White ER, Morin MC, Margueron R, Jarriault S (2014). Sequential histone-modifying activities determines the robustness of transdifferentiation. Science. 345(6198):826-829. 

Wilkinson R, Wang X, Kassianos AJ, Zuryn S, Roper KE, Osborne A, Sampangi S, Francis L, Raghunath V, Healy H (2014). Laser capture microdissection and multiplex-tandem PCR analysis of proximal tubular epithelial cell signaling in human kidney disease. PLoS One. 9(1):e87345.

Zuryn S & Jarriault S (2013). Deep sequencing strategies for mapping and identifying mutations from genetic screens. Worm. 2(3):e25081-10.

Schlipalius DI, Valmas N, Tuck AG, Jagadeesan R, Ma L, Kaur R, Goldinger A, Anderson C, Kuang J, Zuryn S, Mau YS, Cheng Q, Collins PJ, Nayak M, Schirra HJ, Hilliard MA, Ebert PR (2012). A Core metabolic enzyme mediates resistance to phosphine gas. Science. 338(9):807-810.

Zuryn et al 2010. Front cover.

Zuryn S, Daniele T, Jarriault S (2012). Direct cellular reprogramming in C. elegans: facts, models and promises for regenerative medicine. Wiley Interdiscip Rev Dev Biol. 1(1):138-152. 

Richard J*, Zuryn S*, Fischer N, Pavet V, Vaucamps N, Jarriault S (2011). Direct in vivo reprogramming involves transition through discrete, non-pluripotent steps. Development. 138(8):1483-92. (*Co-first)

Zuryn S, Le Gras S, Jamet K, Jarriault S (2010). A strategy for direct mapping and identification of mutants by whole-genome sequencing. Genetics. 186(1):427-30. 

Zuryn S, Kuang J, Tuck A, Ebert PR (2010). Mitochondrial dysfunction in Caenorhabditis elegans causes metabolic restructuring, but this is not linked to longevity. Mech Ageing Dev. 131(9):554-61.

​Zuryn S, Kuang J, Ebert PR (2008). Modulation of mitochondrial phosphine toxicity and resistance in Caenorhabditis elegans. Toxicological Sciences. 102(1):179-86.

​Valmas N*, Zuryn S*, Ebert PR (2008). Mitochondrial uncouplers synergise with the fumigant phosphine to disrupt mitochondrial membrane potential and cause cell death. Toxicology. 30;252(1-3):33-9. (*Co-first)

Dr Steven Zuryn    s.zuryn@uq.edu.au

Please email Dr Zuryn for enquiries about honours and PhD positions.

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