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Exocytosis studied using optical uncaging of PI(4,5)P2

2016-10-17

Professor Jakob B Sörensen,

Institute for Neuroscience and Pharmacology
University of Copenhagen

Friday , October 21, 2016, 11:15, in BMC C8:301


The Sörensen lab is interested in the molecular mechanism of neurotransmitter release in central neurons and in neurosecretory cells. Synaptic vesicles fuse with the plasma membrane to release their content of neurotransmitter. Similarly, neuropeptides and hormones are released through exocytosis of secretory vesicles. We want to understand how exocytosis is executed, which role(s) the presynaptic proteins and lipids play, and how neurotransmitter release is regulated. Finally, we want to understand the link to disease, since aberrant signaling is linked to neuropsychiatric disorders.

Schotten S. (2015). Additive effects on the energy barrier for synaptic vesicle fusion cause supralinear effects on the vesicle fusion rate Elife 4:e05531.

Walter A.M. et al (2014). The SNARE protein vti1a functions in dense-core vesicle biogenesisEMBO J 33,1681-1697.

Mohrmann R., et al (2013). Synaptotagmin interaction with SNAP-25 governs vesicle docking, priming, and fusion triggering. J. Neurosci. 33, 14417-14430.

Mohrmann R., et al (2010). Fast vesicle fusion in living cells requires at least three SNARE-complexesScience 330, 502-505.

Walter A.M. et al (2010).Synaptobrevin N-terminally bound to SNAP-25:syntaxin defines the primed vesicle state in regulated exocytosis. J. Cell Biol. 188, 401-413.

Host: Sebastian Barg (sebastian.barg@mcb.uu.se 018-4714660).