Epigenetics and Mitochondrial Biology Lab


With life expectancies increasing around the world, neurodegenerative disorders 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. 

To sustain correct function, terminally differentiated post-mitotic neurons must preserve their subtype identity, morphology, activity, and connectivity even in the presence of these chronic insults. The Zuryn lab uses cutting-edge molecular genetic techniques in the highly successful model organism C. elegans to understand the fundamental mechanisms neurons use to mitigate disease-related threats. The beauty of such a model is that they are able to accurately distil complex phenotypic phenomena down into single-cell and single-gene resolution. 

In 2015 Dr Zuryn was awarded the Stafford Fox Senior Research Fellowship and opened his new lab at QBI in September. One of the main focuses of the Zuryn group is the emerging role of epigenetic mechanisms that help preserve correct cell function. They have recently found that specific types of histone methylation ensure robust neuronal function in the face of stressful conditions, research that was published in the prestigious journal Science. The team’s next goal is to understand how this occurs, and to be able to predict outcomes under alternative epigenetic criteria that may influence disease progression. 

The Zuryn group is also interested in understanding fundamental aspects of neuronal mitochondrial biology. To do this, they have developed novel genetic tools in 2015 that will allow them to probe neuronal responses under stresses that model stroke and dementia. They aim to develop means to protect robust neuronal function from these types of diseases.



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Group Publications

Research Areas

  • Mitochondrial Biology
  • Epigenetics
  • Neurodegeneration
  • Mitochondrial diseases

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Research Members



Affinity purification of cell-specific mitochondria from whole animals resolves patterns of genetic mosaicism.
Ahier A, Dai CY, Tweedie A, Bezawork-Geleta A, Kirmes I, Zuryn S. Nature Cell Biology. 2018 Jan 22. doi: 10.1038/s41556-017-0023-x. [Epub ahead of print]

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

Wilkinson R., Wang X., Kassianos A.J., Zuryn S., Roper K.E., 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. doi: 10.1371/journal.pone.0087345.

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 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).