Presynaptic dysfunction in drosophila csp mutants
Abstract
Cysteine string proteins are synapse-specific proteins. In Drosophila, csp deletion mutants exhibit temperature-sensitive paralysis and early death. Here, we report that neuromuscular transmission is impaired presynaptically in these csp mutant larvae. At 22°C, evoked transmitter release is depressed relative to wild type and rescued controls, and high frequency stimulation of the nerve leads to sporadic failures. At 30°C, stimulus-evoked responses decline gradually before failing completely. When the temperature is returned to 22°C, evoked responses recover. Spontaneous release events persist at both 22°C and 30°C. Since nerve conduction and postsynaptic sensitivity are unaffected, these data indicate that csp mutations disrupt depolarization-secretion coupling. This disruption explains the cellular basis of the temperature-sensitive paralysis of these organisms.
Additional Information
© 1994 Cell Press. Received 26 May 1994, Revised 20 July 1994. We thank Y. Kidokoro and A. Grinnell for helpful discussions, T. Schwarz and H. Atwood for work in press, and A. Chang and M. Kreman for assistance with figures. Funded by grants from National Institutes of Health J. A. U. and S. B.), National Science Foundation (S. B.), DFG (K. E. Z. and E. B.), and the J. G. Boswell Foundation (S. B.). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement"in accordance with 18 USC Section 1734 solely to indicate this fact.Additional details
- Eprint ID
- 93352
- Resolver ID
- CaltechAUTHORS:20190228-115828203
- NIH
- NSF
- Deutsche Forschungsgemeinschaft (DFG)
- James G. Boswell Foundation
- Created
-
2019-02-28Created from EPrint's datestamp field
- Updated
-
2021-11-16Created from EPrint's last_modified field