Skip to menu Skip to content Skip to footer
Dr Sean Coakley
Dr

Sean Coakley

Email: 
Phone: 
+61 7 336 52873

Overview

Background

I received my PhD from The University of Queensland in 2014 where I studied axonal regeneration and degeneration in the laboratory of Professor Massimo Hilliard at the Queensland Brain Institute. In 2016 I was awarded an NHMRC-ARC Dementia Research Development Fellowship to pursue postdoctoral research in Professor Hilliard's lab with the aim of discovering novel genes that regulate axonal degeneration in C. elegans. In 2018 I was awarded a UQ Early Career Researcher Grant and a Young Tall Poppy Science Award. In 2019 I was a visiting scholar in the laboratory of Professor Kang Shen in the Department of Biology at Stanford University, where I studied how mechanosensitive channels regulate dendrite branching through Ca2+ signaling during neuronal development. In 2022 I was awarded an NHMRC Ideas Grant and was recruited to the School of Biomedical Sciences at UQ as a Group Leader. My lab focuses on understanding the cellular mechanisms that protect the nervous system from damage.

Availability

Dr Sean Coakley is:
Available for supervision

Qualifications

  • Doctoral Diploma of Neurological Sciences, The University of Queensland

Research interests

  • Axonal Degeneration

    Degeneration of the axon, the longest process of a neuron, is a key early pathological hallmark of Neurodegenerative conditions, including motor neuron disease, glaucoma, and Parkinson’s, Huntington’s and Alzheimer’s diseases.  Despite being described more than 100 years ago, we lack a basic understanding of the cellular and molecular mechanisms regulating axonal degeneration. Using the small nematode worm C. elegans, a very powerful genetic model system, we aim to discover molecules with a protective effect on the axon. The results from this study will provide novel and important insights into how axonal degeneration occurs, and how it can be prevented or delayed, potentially leading to the identification of novel molecular targets to treat neurodegenerative disorders.

Research impacts

My laboratory focuses on how to build and maintain a nervous system for life. We use C. elegans as a model system because we can use sophisticated genetic, imaging and molecular approaches to study the cellular mechanisms of neuroprotection in exquisite detail.

Failure to maintain the integrity of the axon, the longest and most susceptible compartment of a neuron, results in compromised neuronal function, which is characteristic of both injury and neurodegenerative diseases. Virtually every neuron, including those of the central nervous system, is susceptible to different types of strain insults such as protein accumulation, vascular accidents, and trauma, with excessive mechanical strain triggering axonal degeneration and progression of neurodegenerative diseases. The molecular mechanisms that maintain axonal integrity are unknown and will be essential to develop neuroprotective therapies for human disorders and injury.

Works

Search Professor Sean Coakley’s works on UQ eSpace

13 works between 2013 and 2025

1 - 13 of 13 works

Featured

2015

Journal Article

EFF-1-mediated regenerative axonal fusion requires components of the apoptotic pathway

Neumann, Brent, Coakley, Sean, Giordano-Santini, Rosina, Linton, Casey, Lee, Eui Seung, Nakagawa, Akihisa, Xue, Ding and Hilliard, Massimo A. (2015). EFF-1-mediated regenerative axonal fusion requires components of the apoptotic pathway. Nature, 517 (7533), 219-222. doi: 10.1038/nature14102

EFF-1-mediated regenerative axonal fusion requires components of the apoptotic pathway

Featured

2013

Journal Article

Rapid and permanent neuronal inactivation in vivo via subcellular generation of reactive oxygen with the use of KillerRed

Williams, Daniel C., El Bejjani, Rachid, Mugno Ramirez, Paula, Coakley, Sean, Kim, Shin Ae, Lee, Hyewon, Wen, Quan, Samuel, Aravi, Lu, Hang, Hilliard, Massimo A. and Hammarlund, Marc (2013). Rapid and permanent neuronal inactivation in vivo via subcellular generation of reactive oxygen with the use of KillerRed. Cell Reports, 5 (2), 553-563. doi: 10.1016/j.celrep.2013.09.023

Rapid and permanent neuronal inactivation in vivo via subcellular generation of reactive oxygen with the use of KillerRed

2025

Journal Article

OSP-1 protects neurons from autophagic cell death induced by acute oxidative stress

Donato, Alessandra, Ritchie, Fiona K., Lu, Lachlan, Wadia, Mehershad, Martinez-Marmol, Ramon, Kaulich, Eva, Sankorrakul, Kornraviya, Lu, Hang, Coakley, Sean, Coulson, Elizabeth J. and Hilliard, Massimo A. (2025). OSP-1 protects neurons from autophagic cell death induced by acute oxidative stress. Nature Communications, 16 (1) 300, 300. doi: 10.1038/s41467-024-55105-0

OSP-1 protects neurons from autophagic cell death induced by acute oxidative stress

2022

Journal Article

Dendrites use mechanosensitive channels to proofread ligand-mediated neurite extension during morphogenesis

Tao, Li, Coakley, Sean, Shi, Rebecca and Shen, Kang (2022). Dendrites use mechanosensitive channels to proofread ligand-mediated neurite extension during morphogenesis. Developmental Cell, 57 (13), 1615-1629.e3. doi: 10.1016/j.devcel.2022.05.019

Dendrites use mechanosensitive channels to proofread ligand-mediated neurite extension during morphogenesis

2022

Journal Article

The metalloprotease ADM-4/ADAM17 promotes axonal repair

Ho, Xue Yan, Coakley, Sean, Amor, Rumelo, Anggono, Victor and Hilliard, Massimo A. (2022). The metalloprotease ADM-4/ADAM17 promotes axonal repair. Science Advances, 8 (11) eabm2882, eabm2882. doi: 10.1126/sciadv.abm2882

The metalloprotease ADM-4/ADAM17 promotes axonal repair

2022

Journal Article

Neuron-epidermal attachment protects hyper-fragile axons from mechanical strain

Bonacossa-Pereira, Igor, Coakley, Sean and Hilliard, Massimo A. (2022). Neuron-epidermal attachment protects hyper-fragile axons from mechanical strain. Cell Reports, 38 (10) 110501, 110501. doi: 10.1016/j.celrep.2022.110501

Neuron-epidermal attachment protects hyper-fragile axons from mechanical strain

2020

Journal Article

Modular transient nanoclustering of activated β2-adrenergic receptors revealed by single-molecule tracking of conformation-specific nanobodies

Gormal, Rachel S., Padmanabhan, Pranesh, Kasula, Ravikiran, Bademosi, Adekunle T., Coakley, Sean, Giacomotto, Jean, Blum, Ailisa, Joensuu, Merja, Wallis, Tristan P., Lo, Harriet P., Budnar, Srikanth, Rae, James, Ferguson, Charles, Bastiani, Michele, Thomas, Walter G., Pardon, Els, Steyaert, Jan, Yap, Alpha S., Goodhill, Geoffrey J., Hilliard, Massimo A., Parton, Robert G. and Meunier, Frédéric A. (2020). Modular transient nanoclustering of activated β2-adrenergic receptors revealed by single-molecule tracking of conformation-specific nanobodies. Proceedings of the National Academy of Sciences of the United States of America, 117 (48), 30476-30487. doi: 10.1073/pnas.2007443117

Modular transient nanoclustering of activated β2-adrenergic receptors revealed by single-molecule tracking of conformation-specific nanobodies

2020

Journal Article

Epidermal control of axonal attachment via β-spectrin and the GTPase-activating protein TBC-10 prevents axonal degeneration

Coakley, Sean, Ritchie, Fiona K., Galbraith, Kate M. and Hilliard, Massimo A. (2020). Epidermal control of axonal attachment via β-spectrin and the GTPase-activating protein TBC-10 prevents axonal degeneration. Nature Communications, 11 (1) 133, 1-12. doi: 10.1038/s41467-019-13795-x

Epidermal control of axonal attachment via β-spectrin and the GTPase-activating protein TBC-10 prevents axonal degeneration

2019

Conference Publication

The metalloprotease ADM-4 promotes regenerative axonal fusion

Ho, X.Y., Coakley, S. and Hilliard, M.A. (2019). The metalloprotease ADM-4 promotes regenerative axonal fusion. International Worm Meeting, UCLA, September. Rockville, MD, United States: Genetics Society of America.

The metalloprotease ADM-4 promotes regenerative axonal fusion

2018

Journal Article

6-OHDA-induced dopaminergic neurodegeneration in Caenorhabditis elegans is promoted by the engulfment pathway and inhibited by the transthyretin-related protein TTR-33

Offenburger, Sarah-Lena, Ho, Xue Yan, Tachie-Menson, Theresa, Coakley, Sean, Hilliard, Massimo A. and Gartner, Anton (2018). 6-OHDA-induced dopaminergic neurodegeneration in Caenorhabditis elegans is promoted by the engulfment pathway and inhibited by the transthyretin-related protein TTR-33. PLoS Genetics, 14 (1) e1007125, 1-27. doi: 10.1371/journal.pgen.1007125

6-OHDA-induced dopaminergic neurodegeneration in Caenorhabditis elegans is promoted by the engulfment pathway and inhibited by the transthyretin-related protein TTR-33

2014

Journal Article

A multi-channel device for high-density target-selective stimulation and long-term monitoring of cells and subcellular features in C. elegans

Lee, Hyewon, Kim, Shin Ae, Coakley, Sean, Mugno, Paula, Hammarlund, Marc, Hilliard, Massimo A. and Lu, Hang (2014). A multi-channel device for high-density target-selective stimulation and long-term monitoring of cells and subcellular features in C. elegans. Lab on a Chip - Miniaturisation for Chemistry and Biology, 14 (23), 4513-4522. doi: 10.1039/c4lc00789a

A multi-channel device for high-density target-selective stimulation and long-term monitoring of cells and subcellular features in C. elegans

2014

Other Outputs

The cellular and molecular mechanisms of axonal maintenance and regeneration

Coakley, Sean (2014). The cellular and molecular mechanisms of axonal maintenance and regeneration. PhD Thesis, Queensland Brain Institute, The University of Queensland. doi: 10.14264/uql.2015.153

The cellular and molecular mechanisms of axonal maintenance and regeneration

2013

Journal Article

A dominant mutation in mec-7/β-tubulin affects axon development and regeneration in Caenorhabditis elegans neurons

Kirszenblat, Leonie, Neumann, Brent, Coakley, Sean and Massimo Hilliard (2013). A dominant mutation in mec-7/β-tubulin affects axon development and regeneration in Caenorhabditis elegans neurons. Molecular Biology of the Cell, 24 (3), 285-296. doi: 10.1091/mbc.E12-06-0441

A dominant mutation in mec-7/β-tubulin affects axon development and regeneration in Caenorhabditis elegans neurons

Funding

Current funding

  • 2025 - 2027
    Discovering how nerve cells resist mechanical forces
    ARC Discovery Projects
    Open grant
  • 2022 - 2025
    A new model of ß-Spectrin function: understanding how the skin protects neurons from damage
    NHMRC IDEAS Grants
    Open grant

Past funding

  • 2018
    Discovering the molecular mechanisms that protect sensory neurons from mechanical damage
    UQ Early Career Researcher
    Open grant
  • 2016 - 2021
    NHMRC-ARC Dementia Fellowship (Aus Based) - Discovering novel molecules that regulate axonal degeneration
    NHMRC-ARC Dementia Research Development Fellowships Scheme
    Open grant

Supervision

Availability

Dr Sean Coakley is:
Available for supervision

Before you email them, read our advice on how to contact a supervisor.

Supervision history

Current supervision

Completed supervision

Media

Enquiries

For media enquiries about Dr Sean Coakley's areas of expertise, story ideas and help finding experts, contact our Media team:

communications@uq.edu.au