Dr Steven Zuryn
Stafford Fox Senior Research Fellow

Contact Information

s.zuryn@uq.edu.au
Building: QBI Building #79
Room: 626
Tel: +61 7 334 66477

Mailing Address

Queensland Brain Institute
The University of Queensland
Brisbane, 4072
Queensland
Australia

Links

Zuryn Lab Website

Short biography

Research directions

Selected publications

 

Short biography

Dr. Steven Zuryn received his PhD under the supervision of Associate Professor Paul Ebert from The University of Queensland, Australia in late 2008. For his thesis work, he investigated mitochondrial mechanisms of toxicity and ageing in the genetic model organism C. elegans. In 2009, he moved to the Institute of Genetics and Molecular Biology, Strasbourg, France to undertake postdoctoral work in the laboratory of Dr. Sophie Jarriault. Here, he further honed his C. elegans skills, developing novel methods to map DNA mutations using deep sequencing and probing the molecular mechanisms underlying transdifferentiation (direct cell conversion). He discovered that modification of histones within transdifferentiating cells was required for extremely precise and robust step-wise conversion of hindgut to motor neuron fate. In September 2015, Steve was appointed as the Stafford Fox Senior Research Fellow and a Group Leader at the Queensland Brain Institute, The University of Queensland. His laboratory investigates epigenetic and mitochondrial biology and is intrigued with the fundamental mechanisms that dictate complex and variable phenotypes.

Research directions

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-onset 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. 

Our 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 we can accurately distil complex phenotypic phenomena down into single cell and single gene resolution.

One of our main focuses is the emerging role of epigenetic mechanisms that help preserve correct cell function. Chromatin was once thought to be only a packaging mechanism for DNA. However, the N-terminal tails of histones undergo a diverse array of post-translational modifications (e.g. methylation, acetylation) that regulate key aspects of chromosome biology. We have recently found that specific types of histone methylation ensure robust neuron function in the face of stressful conditions. Our goal is to understand how, and be able to predict outcomes under alternative epigenetic criteria that may influence disease progression. 

We are also interested in understanding fundamental aspects of neural mitochondrial biology. To do this, we are developing new genetic tools that will allow us probe mitochondrial responses under stresses that model stroke and dementia.

If you are interested in joining the lab, please contact Dr. Steven Zuryn. 

Selected publications 

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).