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How do membranes fuse? How do the mechanisms differ for different classes of neurotransmitter? How do molecular motors control the distribution of organelles? Because of its extraordinarily complex structure and highly regulated mode of exocytosis, the neuron offers special challenges to these and other general cell biological processes.
For example, every cell needs to regulate the number of mitochondria it contains and their distribution within the cell, but in neurons this task is particularly complex because axons can extend over a meter in length from the cell soma, and because different regions of the neuron can have very different energetic demands. Similarly, while every cell has internal membrane traffic and exocytosis at its surface, the neuron needs to regulate the release of neurotransmitter with sub-millisecond timing and with precise control of the number of vesicles to fuse. Therefore, we move back and forth from neurons to non-neuronal cells to understand the fundamental processes of membrane traffic and their specializations in neurons.
Recent projects have also caused us to examine the manner in which signals are communicated from the synapse to the nucleus and the cell biology and signaling events that are required to form a pre-synaptic nerve terminal. This research has also led us to study how compromise of these mechanisms contributes to neurodegeneration.
About Thomas Schwarz
Thomas Schwarz received a PhD in 1983 from the Neurobiology Department of Harvard Medical School. He completed postdoctoral training at the University of California, San Francisco in the laboratory of Lily and Yuh-Nung Jan, where he collaborated in the cloning of the Shaker gene, the first K+ gene to be cloned and sequenced. In 1989, he joined the faculty of Stanford University's Department of Molecular and Cellular Physiology. In 2000, he and his family returned to Boston so that his wife, Sarah Luria, could assume a faculty position in American Literature at the College of the Holy Cross. Tom joined the Harvard faculty as a Professor of Neurology in the F.M. Kirby Neurobiology Center at Children's Hospital, with a joint appointment in the Neurobiology Department of Harvard Medical School. He serves on the Board of Scientific Overseers of the Jackson Laboratory in Bar Harbor, Maine. He also serves on the Board of Trustees of the Jewish Community Day School in Watertown, Mass., and resides with his wife and two children in Newton, MA.
For a full list of Thomas Schwarz's publications on PubMed, click here.
- Chung J.Y., Steen J.A., Schwarz T.L. (2016) Phosphorylation-Induced Motor Shedding Is Required at Mitosis for Proper Distribution and Passive Inheritance of Mitochondria Cell Reports. 16(8):2142-55. doi: 10.1016/j.celrep.2016.07.055. Epub 2016 Aug 11.
- Ashrafi, G., Schlehe, J. S., LaVoie, M. J., & Schwarz, T. L. (2014). Mitophagy of damaged mitochondria occurs locally in distal neuronal axons and requires PINK1 and Parkin. The Journal of Cell Biology, 206(5), 655–670.
- Pekkurnaz, G., Trinidad, J.C., Wang, X., Kong, D. and Schwarz, T.L. (2014). Glucose Regulates Mitochondrial Motility via Milton Modification by O-GlcNAc Transferase. Cell, 158:54-68.
- Teodoro, R.O., Pekkurnaz, G., Nasser, A., Higashi-Kovtun, M.E., Balakireva, M., McLachlan, I.G., Camonis, J., and Schwarz, T.L. (2013) Ral mediates activity-dependent growth of postsynaptic membranes via recruitment of the exocyst. EMBO J. 32: 2039-55.
- Wang, X., Winter, D., Ashrafi, G., Schlehe, J., Wong, Y.L., Selkoe, D., Rice, S.J., Steen, J., LaVoie, M.J., and Schwarz, T.L. (2011) PINK1 and Parkin target Miro for phosphorylation and degradation to arrest mitochondrial motility. Cell 147:893-907.
- Mosca, T.J. and Schwarz, T.L. (2010) The nuclear import of Frizzled2-C by Importins beta11 and alpha2 promotes postsynaptic development. Nat Neurosci. 66:624-7.
- Kurshan, P.T., Oztan, A. and Schwarz, T.L. (2009) Presynaptic α2δ-3 protein is required for synaptic morphogenesis independent of its Ca++-channel functions. Nature Neuroscience 12:1411-1419. Wang, X. and Schwarz, T.L. (2009) The mechanism of Ca++ regulation of kinesin-mediated mitochondrial motility. Cell 136:163-174.
- Pack-Chung, E., Kurshan, P.T., Dickman, D.K., and Schwarz, T.L. (2007) A Drosophila Kinesin Required for Synaptic Bouton Formation and Synaptic Vesicle Transport. Nature Neuroscience 10:980-989.
- Dickman, D.K, Horne, J.A., Meinertzhagen, I.A., and Schwarz, T.L. (2005) A slowed classical pathway rather than kiss-and-run mediates endocytosis at synapses lacking synaptojanin and endophilin. Cell 123:521-533.