Deciphering the role of atypical DNA methylation in activity-dependent neuronal maturation

​DNA methylation (mC) is a covalent modification in post-mitotic cells that has been implicated in neural plasticity. Although methylation of DNA in the context of CG (on the cytosine of CpG dinucleotides) is a well-established, epigenetic mechanism regulating gene expression, it has more recently been shown that DNA methylation can also occur in the CH context, where H=A, T or C. Post-natal accumulation of mCH has been found to occur in the brain of both mice and humans shortly after birth, where it is enriched in neurons, suggesting a role in neuronal maturation linked to increased sensory input. In this study Dr Martin is investigating the hypothesis that mCH is aregulatory mechanism by which stable but reversible patterns of gene expression can be established in mature neurons, using neuron derived from mouse and human PSCs.

Dr Sally Martin's research interests lie in the mechanisms underlying cell metabolism and cell differentiation in normal conditions and disease states. After graduating in the UK, she moved to the University of Queensland where she established a strong, consistent track record as a molecular cell biologist at the IMB. She subsequently moved to the Queensland Brain Institute (QBI) to develop her understanding of neuronal cell biology, and to the AIBN to utilize this understanding in the generation of neurons from PSCs. Technically she has direct experience in a large number of state of the art cell biological techniques, including advanced light and electron microscopy (including TIRF microscopy and electron tomography), proteomic analyses (including SILAC), cell-based high content automated screening and RNAi-based protein knock down.

Industry Engagement and Collaborations

Dr Martin's primary research collaborations are with Prof Ryan Lister at UWA and Assoc Prof Jose Polo at Monash Monash University.


​As Chief Investigator A or B, Dr Martin has successfully attracted over $900K in research funding through seven independent grants, from both government and independent funding bodies. She has been an integral part of two NHMRC Program grants as a Co-Investigator, which together totaled over $11.8M

Key Publications

  1. ​*Wang, T.,*Martin, S., Nguyen, T.H., Harper, C.B., Gormal, RS.., Martinez-Marmol, R., Karunanithi, S., Coulson, E.J., Glass, N.R., Cooper-White, J.J., van Swinderen, B., Meunier, F.A. (2016) Flux of signalling endosomes undergoing axonal retrograde transport is encoded by presynaptic activity and TrkB. Nature Comm. 7:12976 *co-first authors
  2. Wang, T., Martin, S., Papadopulos, A., Harper, C.B., Mavlyutov, T.A., Niranjan, D., Glass, N.R., Cooper-White, J.J., Sibarita, J.B., Choquet, D., Davletov, B., and Meunier F.A. (2015) Control of autophagosome axonal retrograde flux by presynaptic activity unveiled using botulinum neurotoxin type a. J. Neurosci. 35: 6179-6194
  3. Papadopulos, A., Gomez, G.A., Martin, S., Jackson, J., Keating, D.J., Gormal, R.S., Yap, A.S., Meunier, F.A. (2015) Activity-driven relaxation of the cortical acto-myosin II network synchronizes Munc18-1-dependent neurosecretory vesicle docking. Nature Comm. 6:6297
  4. Martin, S., Papadopulos, A., Tomatis, V.M., Sierecki, E., Malintan, N.T., Gormal, R.S., Giles, N., Johnston, W.A., Alexandrov, K., Gambin, Y., Collins, B.M., and Meunier, F.A. (2014) Munc18-1 disease-linked mutation potentiates polyubiquitination and proteasomal degradation leading to temperature sensitive defect in neuroexocytosis. Cell Reports 9:206-218
  5. Martin, S., Tomatis, V.M., Papadopulos, A., Christie, M.P., Malintan, N.T., Gormal, R.S., Sugita, S., Martin, J.L., Collins, B.M. and Meunier, F.A. (2013) The Munc18-1 domain 3a loop is essential for neuroexocytosis but not for Syntaxin1A transport to the plasma membrane. J Cell Sci 126:2353-2360