Note to users. If you're seeing this message, it means that your browser cannot find this page's style/presentation instructions -- or possibly that you are using a browser that does not support current Web standards. Find out more about why this message is appearing, and what you can do to make your experience of our site the best it can be.


Sci. Signal., 11 May 2010
Vol. 3, Issue 121, p. ec144
[DOI: 10.1126/scisignal.3121ec144]


Neuroscience A Trick of the Tail

Stella M. Hurtley

Science, AAAS, Cambridge CB2 1LQ, UK

The synaptic vesicle protein, synaptotagmin 1 (Syt1), acts as the main Ca2+-dependent switch for neurotransmitter release. In vitro studies of the truncated Syt1, which lacks the transmembrane domain, have unveiled the fusion-triggering mechanism of Syt1. However, in vitro approaches using the full-length, membrane-anchored Syt1 have not only failed to recapitulate Ca2+-triggered membrane fusion but could even inhibit vesicle fusion. In contrast, the membrane anchor is conserved across the Syt family, suggesting a critical functional role for the membrane anchor. Now, using a single-vesicle fusion assay, H.-K. Lee et al. show that the membrane anchor is indeed essential for Syt1 to induce physiological rates of Ca2+-induced vesicle fusion on a 100-millisecond time scale.

H.-K. Lee, Y. Yang, Z. Su, C. Hyeon, T.-S. Lee, H.-W. Lee, D.-H. Kweon, Y.-K. Shin, T.-Y. Yoon, Dynamic Ca2+-dependent stimulation of vesicle fusion by membrane-anchored synaptotagmin 1. Science 328, 760–763 (2010). [Abstract] [Full Text]

Citation: S. M. Hurtley, A Trick of the Tail. Sci. Signal. 3, ec144 (2010).

To Advertise     Find Products

Science Signaling. ISSN 1937-9145 (online), 1945-0877 (print). Pre-2008: Science's STKE. ISSN 1525-8882