Dion Kai Dickman
- Synapse development, function, and plasticity in Drosophila
Research OverviewWe are interested in synapse development, function, and plasticity in general, and in particular how these processes are stably maintained within proper physiological ranges, referred to as homeostatic synaptic plasticity. Homeostatic feedback systems are a ubiquitous form of biological regulation, which recently have been demonstrated to maintain the stability of nervous system function. Homeostatic processes also play crucial roles in the development of the nervous system, tuning synaptic strength and establishing the proper balance of excitation and inhibition. Dysfunction in these systems may contribute to the etiology of schizophrenia, autism, epilepsy, and other complex neurological and psychiatric diseases. Our long term interests are to identify the molecules and elucidate the mechanisms that achieve and maintain the stability of neural function, and to determine how dysfunction in these processes may contribute to human disease.
We use the fruit fly Drosophila melanogaster as a model system because of its amenability to advanced genetic, molecular, electrophysiological, imaging, and cell biological approaches. Using an electrophysiology-based forward genetic screen, we have isolated several novel genes that are required for adaptive plasticity, including one, dysbindin, which has been linked to schizophrenia in humans. We are currently characterizing other novel genes and performing further screens with the goal of illuminating the molecular, cellular, and synaptic mechanisms governing this complex, fundamental and poorly understood process.
University Park Campus
3641 Watt Way
HNB 309 M/C 2520
Los Angeles, CA 90089-2520
- PhD, Harvard University
- Post-doctoral training: UCSF
Selected PublicationsView a complete PubMed searchView a complete Google Scholar search
Chen X, Ma W, Zhang S, Paluch J, Guo W, Dickman DK.
eNeuro. 2017 Feb 8;4(1). pii: ENEURO.0335-16.2017. doi: 10.1523/ENEURO.0335-16.2017. eCollection 2017 Jan-Feb.
Robinson JE, Paluch J, Dickman DK, Joiner WJ.
Nat Commun. 2016 Jan 27;7:10512. doi: 10.1038/ncomms10512.
Harris N, Braiser DJ, Dickman DK, Fetter RD, Tong A, Davis GW.
Neuron. 2015 Dec 16;88(6):1157-64. doi: 10.1016/j.neuron.2015.10.049.
Mullin AP, Sadanandappa MK, Ma W, Dickman DK, VijayRaghavan K, Ramaswami M, Sanyal S, Faundez V.
J Neurosci. 2015 Jan 7;35(1):325-38. doi: 10.1523/JNEUROSCI.3542-14.2015.
Perry S, Kiragasi B, Dickman D, Ray A.
Cell Rep. 2017 Feb 7;18(6):1337-1345. doi: 10.1016/j.celrep.2017.01.028.
- New approaches for studying synaptic development, function, and plasticity using Drosophila as a model system. Frank CA, Wang X, Collins CA, Rodal AA, Yuan Q, Verstreken P, Dickman DK.
J Neurosci. 2013 Nov 6;33(45):17560-8. doi: 10.1523/JNEUROSCI.3261-13.2013.PubMed
Wondolowski J, Dickman D.
Front Cell Neurosci. 2013 Nov 21;7:223. doi: 10.3389/fncel.2013.00223.
Chen CK, Bregere C, Paluch J, Lu JF, Dickman DK, Chang KT.
Nat Commun. 2014 Jun 30;5:4246. doi: 10.1038/ncomms5246.
Wang T, Hauswirth AG, Tong A, Dickman DK, Davis GW.
Neuron. 2014 Aug 6;83(3):616-29. doi: 10.1016/j.neuron.2014.07.003.
Dickman DK, Tong A, and Davis, GW (2012). Snapin is critical for presynaptic homeostatic plasticity. Journal of Neuroscience 32(25): 8716-24.
Bergquist S, Dickman DK, and Davis GW (2010). A hierarchy of cell intrinsic and target-derived homeostatic signaling. Neuron 66(2): 220-234.PubMed
Dickman DK and Davis GW (2009). The schizophrenia susceptibility gene dysbindin controls synaptic homeostasis. Science 326(5956): 1127-1130.
Dickman* DK, Kurshan* P, and Schwarz TL (2008). Mutations in a Drosophila Î±2Î´ voltage-gated calcium channel subunit reveal a crucial synaptic function. Journal of Neuroscience 28(1): 31-38. * Equal contributionPubMed
Dickman DK, Lu Z, Meinertzhagen IA, and Schwarz TL (2006). Altered synaptic development and active zone spacing at the neuromuscular junctions of endocytosis mutants. Current Biology 16: 591-598.PubMed
Dickman DK, Horne JA, Meinertzhagen IA, and Schwarz TL (2005). A slowed classical pathway rather than kiss-and-run mediates endocytosis at synapses lacking synaptojanin and endophilin. Cell 123: 521-533.PubMed
Gokhale A, Hartwig C, Freeman AH, Das R, Zlatic SA, Vistein R, Burch A, Carrot G, Lewis AF, Nelms S, Dickman DK, Puthenveedu MA, Cox DN, Faundez V.
J Neurosci. 2016 Dec 7;36(49):12393-12411.