Group leader: Patrik Verstreken

PhD: Baylor Coll. of Medicine, Houston, USA, '03
Postdoc: Howard Hughes Medical Inst., BCM, Houston, USA, '03-'06
VIB Group leader since 2007

Research interests

In the laboratory of neuronal communication we aim to understand the molecular mechanisms of neurotransmission at live synapses. Such studies will eventually allow us to elucidate how alterations in transmitter release control complex behaviours, ultimately directing how our brain operates. Neurons talk to one another using small transmitter filled synaptic vesicles that fuse with the neuron membrane to release neurotransmitters activating the next cell in line. During intense stimulation, many vesicles are used and to ensure reliable communication, neurons massively recycle vesicles at their synaptic endings.
In the laboratory of neuronal communication we will address key aspects of neuronal function. For example, we are assessing the role of lipids in synaptic vesicle recycling and we are studying how synaptic mitochondria affect transmitter release in normal and diseased synapses. We are also performing genetic screens to identify novel components involved in vesicle recycling and neurological disease such as Parkinson’s. Given that altered synaptic communication is thought to be one of the leading causes of several deleterious neurological and psychiatric disorders, our studies will have significant implications for human mental health.

To study the molecular mechanisms of synaptic function in vivo, we are using a genetic approach using fruit flies as a model, screening for mutations in critical genes and revealing their function by studying mutant phenotypes. Flies are well suited to study the mechanisms underlying synaptic function since all key synaptic proteins identified in humans also exist in flies, and they show on average 75% protein similarity to their mammalian counterparts. Given the experimental advantages, flies are an ideal system to study vesicle recycling. In particular, we use the larval neuromuscular junction to combine Drosophila genetics with electrophysiology, electron microscopy, immunohistochemistry, calcium imaging, live dye uptake and release studies, and pharmacological inhibition of synaptic processes. In addition, we are implementing novel technologically advanced imaging techniques to study the mechanisms of synaptic plasticity. The ability to apply these assays to one single synapse is unique and very powerful, allowing us to propose very specific functions for the proteins studied.

More info on our Lab Website

Schedule Fly Meetings: FlyMeetings-2011-2012.xlsx

Key Publications

• Valerie Uytterhoeven, Sabine Kuenen, Jaroslaw Kasprowicz, Katarzyna Miskiewicz and Patrik Verstreken. (2011). Loss of Skywalker reveals synaptic endosomes as sorting stations for synaptic vesicle proteins. Cell. 146:117-132.(Abstract).
• Thang-Mahn Khong, Ron L.P. Habets, Jan Slabbaert and Patrik Verstreken. (2010). Wiscott-Aldrich Syndrome Protein is activated by PI(4,5)P2 to restrict neuromuscular junction growth in a pathway parallel to BMP signaling. Proceedings of the National Academy of Sciences. 107:17379-17384. (Abstract)
• Patrik Verstreken, Tomoko Ohyama, Claire Haueter, Ron L.P. Habets, Yin Q. Lin, Laura E. Swan, Cindy V. Ly, Koen J. Venken, Pietro De Camilli and Hugo J. Bellen. (2009). Tweek, an evolutionarily conserved protein, is required for synaptic vesicle recycling. Neuron, 63:203-215.(Abstract)
• Ching Man Choi, Sven Vilain, Sofie Van Kelst, Marion Langen, Nathalie De Geest, Jiekun Yan, Patrik Verstreken and  Bassem A. Hassan. (2009). Conditional mutagenesis in Drosophila. Science, 324:54. (Abstract)
• Vanessa A. Morais, Patrik Verstreken, Anne Röthig, Joél Smet, An Snellinx, Dominik M. Haddad, Wim Mandemakers, Rudy Van Coster, Wolfgang Wurst, Luca Scorrano and Bart De Strooper (2009). Parkinson’s disease mutations in PINK1 affect Complex I activity in mitochondria. EMBO Molecular Medicine, 1:99-111.(Abstract)
• Jaroslaw Kasprowicz, Sabine Kuenen, Ron Habets, Katarzyna Miskiewicz, Liesbet Smitz and Patrik Verstreken. (2008). Inactivation of clathrin heavy chain inhibits synaptic recycling but allows bulk membrane uptake. The Journal of Cell Biology, 182:1007-1016.(Abstract)
• Koen J.T. Venken, Jaroslaw Kasprowicz, Sabine Kuenen, Jiekun Yan, Bassem Hassan and Patrik Verstreken. (2008). Recombineering-mediated tagging of Drosophila genomic constructs for in vivo localization and acute protein inactivation. Nucleic Acids Research, 36:e114, 1-9.(Abstract)
• Patrik Verstreken, Cindy V. Ly, Koen J.T. Venken, Tong-Wey Koh, Yi Zhou and Hugo J. Bellen (2005). Synaptic mitochondria are critical for mobilization of the reserve pool vesicles at the Drosophila neuromuscular junction. Neuron, 47:365-378.(Abstract)
• Patrik Verstreken, Tong-Wey Koh, Karen L. Schulze, R. Grace Zhai, P. Robin Hiesinger, Yi Zhou, Sunil Q. Mehta, Yu Cao, Jack Roos, and Hugo J. Bellen (2003). Synaptojanin is recruited by Endophilin to promote synaptic vesicle uncoating. Neuron, 40:733-748.(Abstract)
• Patrik Verstreken, Ole Kjaerulff, Thomas E. Lloyd, Richard Atkinson, Yi Zhou, Ian A. Meinertzhagen, and Hugo J. Bellen. (2002). Endophilin mutations block clathrin-mediated endocytosis but not neurotransmitter release. Cell 109:101-112.(Abstract)
  

Positions Available

PhD and Post Doc positions available: If you are interested to join a motivated and interactive group of researchers interested in neuronal communication, please contact us by email or telephone +32 (0)16 330018.

Research Team