Epigenetics and Mitochondrial Biology.
Queensland Brain Institute, The University of Queensland
About Us
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 a hallmark of 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 stressors ultimately lead to a decline in individual neuron function over time.
The Zuryn lab uses cutting-edge molecular and cellular techniques in C. elegans and human cell culture systems to understand the fundamental mechanisms by which cells respond to and mitigate 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 more than others (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 Cell Reports 2021).
Excitingly, the Zuryn lab are now uncovering multiple distinct 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 (Dai et al. Nature Cell Biology 2023).
Furthermore, they have revealed an ancient epigenetic mark (6mA) that decorates the mtDNA and protects against the inheritance of mtDNA mutations to future generations (Hahn et al. Cell Metabolism 2024).
The overarching aim of the Zuryn lab is to discover new molecules and mechanisms that protect cells from the effects of mitochondrial dysfunction and that may be used as novel therapeutics to counteract mitochondrial and neurodegenerative disease.
The Zuryn lab uses cutting-edge molecular and cellular techniques in C. elegans and human cell culture systems to understand the fundamental mechanisms by which cells respond to and mitigate 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 more than others (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 Cell Reports 2021).
Excitingly, the Zuryn lab are now uncovering multiple distinct 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 (Dai et al. Nature Cell Biology 2023).
Furthermore, they have revealed an ancient epigenetic mark (6mA) that decorates the mtDNA and protects against the inheritance of mtDNA mutations to future generations (Hahn et al. Cell Metabolism 2024).
The overarching aim of the Zuryn lab is to discover new molecules and mechanisms that protect cells from the effects of mitochondrial dysfunction and that may be used as novel therapeutics to counteract mitochondrial and neurodegenerative disease.
Announcements
Highlights
January 2026: We welcome our new undergrad summer students to the lab, Maya and Jack! They are supervised by Dan and Anne, respectively. (Left to right: Anne, Jack, Maya, Dan)
January 2026: Hear Steve and Tessa on the latest QBI podcast.
December 2025: Congratulations to Tessa for The Joan Lawrence Endowment Prize for High-Achieving Women in Neuroscience.
March 2025: Michael gives his last talk to QBI before his next exciting chapter at Harvard University! The talk was on protecting cells from genetic damage.
December 2024: Anne Hahn wins the 'QBI Best Student Research Paper' award. Congratulations!
October 2024: Michael publishes a helpful tool for finding the right genetic markers.
22 August 2024: How and which mitochondrial mutations might be inherited? Congratulations to Anne Hahn for a publication in Cell Metabolism. Well done!
8 July 2024: SUSTech-UQ Joint Centre for Neuroscience and Neural Engineering Symposium. Today, we also welcome a Masters student, Yixin.
July 2024: Congratulations to Steve, who was awarded the Ross Crozier Medal for outstanding contributions to the field of genetics research by mid-career Australasian scientist.
6 November 2023: Chai Chee is conferred! Congratulations, Dr Ng :D
23 October 2023: We welcome Sasheen to the lab as a research assistant.
23 August 2023: Steve was awarded an ARC Future Fellowship! This will fund important research into the microbiome and mitochondria.
18 July 2023: Michael's new paper is out in Nature Cell Biology! Click here to see it.
14 July 2023: Congratulations to Dan for being awarded the University Medal for an oustanding BAdSc(Hons) degree!
24 - 28 June 2023: Chai Chee and Anne attended the 24th International C. elegans Conference.