Drosophila Hsc70-4 is critical for neurotransmitter exocytosis in vivo

Peter Bronk, Julia J. Wenniger, Ken Dawson-Scully, Xiufang Guo, Susie Hong, Harold L. Atwood, Konrad E. Zinsmaier

Research output: Contribution to journalArticlepeer-review

88 Scopus citations

Abstract

Previous in vitro studies of cysteine-string protein (CSP) imply a potential role for the clathrin-uncoating ATPase Hsc70 in exocytosis. We show that hypomorphic mutations in Drosophila Hsc70-4 (Hsc4) impair nerve-evoked neurotransmitter release, but not synaptic vesicle recycling in vivo. The loss of release can be restored by increasing external or internal Ca2+ and is caused by a reduced Ca2+ sensitivity of exocytosis downstream of Ca2+ entry. Hsc4 and CSP are likely to act in common pathways, as indicated by their in vitro protein interaction, the similar loss of evoked release in individual and double mutants, and genetic interactions causing a loss of release in trans-heterozygous hsc4-csp double mutants. We suggest that Hsc4 and CSP cooperatively augment the probability of release by increasing the Ca2+ sensitivity of vesicle fusion.

Original languageEnglish (US)
Pages (from-to)475-488
Number of pages14
JournalNeuron
Volume30
Issue number2
DOIs
StatePublished - 2001

ASJC Scopus subject areas

  • Neuroscience(all)

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