Building bridges in communication

Our group succeeded in elucidating the mechanism of rapid signal transmission between neurons. This work, published in the current issue of the renowned journal nature neuroscience, shows that a special protein, the so-called "synaptotagmin" (Syt 1), is responsible for the high speed through bridging.

The communication between nerve cells forms the essential basis of the function of our brain. The signal transmission takes place via highly complex contact points, the synapses. Incoming signals cause substances to be released from so-called vesicles. These merge with the adjacent cell membrane to relay the signal. However, the vesicles can only fuse with the membrane if both get close enough. Speed is everything.
"In summary, the distance between the synaptic vesicle and the membrane is a major obstacle and prevents rapid fusion," says Prof. Christian Rosenmund. Previously, it was known that the protein synaptotagmin plays an important role in the speed of signal transduction, but the exact mechanism remained unclear. "We have now found that synaptotagmin can pull synaptic vesicles to the membrane within milliseconds, bridging the vesicle and membrane like a double-sided tape." Only with this bridge in place the fusion can proceed quickly, the researchers write.
Fundamental for these findings was a novel electron microscopic technique developed in the Rosenmund lab, which now allows the researchers to resolve the millisecond structural dynamics in the nerve endings in a slow-motion manner. Actually - not uncommon in basic biological research - these new findings were a chance discovery. Shuwen Chang, who works in the Rosenmund lab and was the lead author of the study, was to use the novel electron microscopic method to directly observe the process of vesicle-membrane fusion. "Because this process is so fast, we looked at ways we could slow down the fusion," Dr. Chang said. We came up with the idea to slow down the fusion by removing synaptotagmin. What we then surprisingly observed was that the lack of synaptotagmin not only slowed down the fusion but also distanced the vesicle and membrane."
Meanwhile, clinical studies discovered that mutations of synaptotagmin can also cause neurological diseases. The Rosenmund lab will now test whether these mutations also alter the rate of vesicle fusion and thus impair nerve cell communication.
Original publication 
Shigeki Watanabe recieves the Kazato Prize from the Kazato Research Foundation in Japan

June 2016

The Prize Jury 

selected Shigeki Watanabe, Assistant Professor, Department of Cell Biology, School of Medicine, Johns Hopkins University

as the winner of the Kazato Prize.



Shigeki Watanabe receives Eppendorf & Science Prize for Neurobiology

Sept. 2015

The Prize Jury chaired by Dr. Peter Stern, Science Senior Editor, 

selected Shigeki Watanabe, post-doctoral fellow, University of Utah &

Charité – Universitätsmedizin Berlin as the 2015 winner of the

Eppendorf & Science Prize for Neurobiology.

Shigeki Watanabe born in 1981 receives the US$25,000 research prize for his work on synaptic vesicle endocytosis.



Shigeki Watanabe receives prestigious award from the German Society for Physiology!

Mar. 2015Christian, Shigeki and Volkmar Leßmann

Shigeki Watanabe, a post-doctoral fellow in our lab, was honored at the 2015 German Society for Physiology meeting in Magdeburg. He and his collaborators have recently discovered a new mechanism of synaptic vesicle recycling using a novel electron microscopy technique, "flash-and-freeze".



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