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First published online 30 January 2007
doi: 10.1242/jcs.03375

Journal of Cell Science 120, 617-627 (2007)
Published by The Company of Biologists 2007
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Research Article

Synaptotagmins I and IX function redundantly in regulated exocytosis but not endocytosis in PC12 cells

Kara L. Lynch and Thomas F. J. Martin*

Department of Biochemistry, 433 Babcock Drive, University of Wisconsin, Madison, WI 53706, USA

* Author for correspondence (e-mail: tfmartin{at}wisc.edu)

Accepted 7 December 2006

Synaptotagmin I is considered to be a Ca2+ sensor for fast vesicle exocytosis. Because Ca2+-dependent vesicle exocytosis persists in synaptotagmin I mutants, there must be additional Ca2+ sensors. Multiple synaptotagmin isoforms co-reside on vesicles, which suggests that other isoforms complement synaptotagmin I function. We found that full downregulation of synaptotagmins I and IX, which co-reside on vesicles in PC12 cells, completely abolished Ca2+-dependent vesicle exocytosis. By contrast, Ca2+-dependent exocytosis persisted in cells expressing only synaptotagmin I or only synaptotagmin IX, which indicated a redundancy in function for these isoforms. Although either isoform was sufficient to confer Ca2+ regulation on vesicle exocytosis, synaptotagmins I and IX conferred faster and slower release rates, respectively, indicating that individual isoforms impart distinct kinetic properties to vesicle exocytosis. The downregulation of synaptotagmin I but not synaptotagmin IX impaired compensatory vesicle endocytosis, which revealed a lack of isoform redundancy and functional specialization of synaptotagmin I for endocytic retrieval.

Key words: Synaptotagmin, Exocytosis, Membrane fusion, Ca2+ sensor, Dense-core vesicles


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