Rhee, Jeong Seop, Prof. Dr.

Professor, Max Planck Institute for Multidisciplinary Sciences

  • M.S. in Biology, Sogang University Master thesis, Seoul, Korea (1992)
  • Ph. D. Kyushu University, School of Medicine Department of Physiology, Japan (1997)
  • Assistant Professor, Kyushu University, Faculty School of Medicine Department of Physiology, Japan (1997-2000)
  • Postdoctoral fellow, Max-Planck Institute Biophysical Chemistry, Department of Membranbiophysik, Germany (2000-2004)
  • Assistant Professor, Baylor College of Medicine, Department of Human Genetics and Neuroscience, USA (2004-2006)
  • Group Leader, Max Planck Institute of Experimental Medicine, Göttingen, Germany (since 2006)
  • Professor, University of Göttingen, Germany (since 2017)

Major Research Interests

Neurophysiology Group

We study that signaling between nerve cells in the brain is mainly mediated at synapses, which are specialized cellular contact sites. The transfer of information at synapses can be regulated dynamically, a process that is called synaptic plasticity. Our main research goal is to elucidate the molecular mechanisms that underlie synaptic plasticity at synapses in the central nervous system. For this purpose we mainly use electrophysiological methods, in combination with nerve cells from genetically modified mice or virus-mediated molecular perturbation of nerve cell function.

Neurotransmitter release is the first step in synaptic signaling. It is mediated by exocytosis of synaptic vesicles at highly specialized contact sites, the active zones of synapses. Neurotransmitters are stored in synaptic vesicles, which undergo a complex trafficking cycle in the presynaptic compartment in order to sustain the rapid and repetitive transfer of information between nerve cells. Synaptic vesicles are initially tethered at the active zone plasma membrane, a process termed docking. Subsequently vesicles undergo a prefusion reaction termed priming, which renders docked vesicles fusion competent, thus defining the readily releasable pool of vesicles. Triggered by the arrival of an action potential at the nerve terminal and the concomitant increase in the intracellular Ca2+ concentration, a fraction of fusion competent vesicles in the readily releasable pool fuse with the plasma membrane and release their content. After fusion, vesicular membrane and protein components are recycled by endocytosis and used for additional rounds of exocytosis.

Essentially, each step of the synaptic vesicle cycle can contribute to the regulation of synaptic plasticity. We combine mouse genetics, molecular biological and morphological methods, and patch clamp electrophysiological analyses of autaptic cultured neurons, organotyptic brain slice cultures, acute brain slices, or acutely isolated neurons with active presynaptic terminals in order to identify the molecular mechanisms underlying the individual synaptic vesicle recycling steps. In the past, we characterized mutant mice lacking identified presynaptic protein components of the neurotransmitter release machinery. Experiments on mutant mouse neurons are complemented by virus mediated expression of proteins in cultured neurons, which allows us to perform detailed structure-function analyses of presynaptic proteins.

Selected Recent Publications

  • Lai Y, Choi UB, Leitz J, Rhee HJ, Lee C, Altas B, Zhao M, Pfuetzner RA, Wang A, Brose N, Rhee JS and Brunger AT (2017) Molecular mechanisms of synaptic vesicle priming by Munc13 and Munc18. Neuron, in press
  • Sigler A, Oh WC, Imig C, Altas B, Kawabe H, Cooper BH, Kwon HB, Rhee JS*, Borse N* (2017) Formation and Maintenance of Functional Spines in the Absence of Presynaptic Glutamate Release. Neuron 94; 304-311: (*joint corresponding authors
  • Kawabe H, Mitkovski M, Kaeser PS, Hirrlinger J, Opazo F, Nestvogel D, Kalla S, Fejtova A, Verrier SE, Bungers SR, Cooper BH, Varoqueaux F, Wang Y, Nehring RB, Gundelfinger ED, Rosenmund C, Rizzoli SO, Südhof TC, Rhee JS, Brose N (2017) ELKS1 localizes the synaptic vesicle priming protein bMunc13-2 to a specific subset of active zones. J Cell Biol. 216;1205
  • Ripamonti S, Ambrozkiewicz MC, Guzzi F, Gravati M, Biella G, Bormuth I, Hammer M, Tuffy LP, Sigler A, Kawabe H, Nishimori K, Toselli M, Brose N, Parenti M, Rhee J (2017) Transient Oxytocin signaling primes the development and function of excitatory hippocampal neurons. Elife doi:10.7554/eLife 22466
  • Mortensen LS, Park SL, Ke J, Cooper BH, Zhang L, Imig C, Löwel S, Reim K, Brose N, Demb JB, Rhee JS*, Singer JH* (2016) Complexin 3 increases the fidelity of signaling in a retinal circuit by regulating exocytosis at ribbon synapses. Cell Rep, in press. (*joint corresponding authors)