Associate Professor Peter Noakes

Associate Professor

School of Biomedical Sciences
Faculty of Medicine
+61 7 336 51780
+61 7 336 51640


Research Interests

    The cell and molecular mechanisms that underlie developmental motoneuron cell death. This involves examining a number of genetically modified mice that we and our colleagues have created. In each of these mice we have inactivated the genes that encode for synaptic signalling molecules, such as agrin and laminins, or molecules that are needed to cluster ion channels in the postsynaptic membranes of muscles and/or neurones, such as rapsyn and gephyrin.
    The molecular mechanisms that underpin synapse formation and plasticity. This involves exploring the signal transduction mechanisms that are activated when signalling molecules such as neuregulin-1 (ARIA, beta-heregulin 1), or agrin active ErbB or MuSK receptors in the membrane of muscle respectively.
    The biological role of P2X1, 2, 4 and 7 in the living animal. This is big project and involves making tissue inducible gene knockouts of these ion channels. At present we are well on the way to making such mice. However, before we can gain a proper understanding of their role in mice that are missing these ion channel subunits, we need to know their developmental expression profile in the developing mouse. In particular when and where they are expressed in the developing nervous system.
    The biological role of TGFbeta 2 at adult synapses. This will involve looking at mice we are making where we the gene for TGFbeta is knockout out in adult muscle and/or in the adult spinal cord (a tissue inducible knockout out of TGFbeta 2). The mice should be ready sometime next year but no firm dates for this one.
    The Control of synaptic gene expression. This project in the first part is simply a promoter and 3' UTR analysis of some 30 genes that appear at the same time in the postsynaptic region of skeletal muscle. It is aimed at looking for common regulatory elements and or spacing patterns of such elements (enhancers and repressors). It is high risk and involves some biological and mathematical knowledge. The biological part of this project will involve making transgenic mice with test non-coding DNA linked to reporter constructs such as green fluorescent protein (GFP). The aim here is to see if such elements can drive synapse expression of reporter genes (eg GFP)
    The roles of insulin-like growth factors 1 and 2 (IGF-1, IGF-2), as well as insulin. in the proliferation and differentiation of mouse embryonic stem cells. This is not a neurobiology-based project, but is early developmental biology one. It will also have links through our USA collaborators to understanding the role of such growth factors in the proliferation tumor cells within the brain (U87 a nasty brain tumor). In particular, this project is aimed at looking at the signalling pathways that are activated when these growth factors activate their receptors, which are on these stem and tumor cells. We also want to know if these signalling pathways activate proliferation and differentiation. And if so what are the down stream target genes involved.


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  • Doctor Philosophy

  • Doctor Philosophy

  • Doctor Philosophy

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Book Chapter

  • Lee, John D., Lee, Jia Y., Taylor, Stephen M., Noakes, Peter G. and Woodruff, Trent M. (2012). Innate immunity in ALS. Amyotrophic lateral sclerosis. (pp. 393-412) edited by Martin H. Maurer. Croatia: InTech - Open Access Publisher. doi: 10.5772/30341

Journal Article

Conference Publication

Grants (Administered at UQ)

PhD and MPhil Supervision

Current Supervision

Completed Supervision