Synaptic transmission persists in synaptotagmin mutants of Drosophila

Cell. 1993 Jul 2;73(7):1281-90. doi: 10.1016/0092-8674(93)90356-u.

Abstract

Synaptotagmin is one of the major integral membrane proteins of synaptic vesicles. It has been postulated to dock vesicles to their release sites, to act as the Ca2+ sensor for the release process, and to be a fusion protein during exocytosis. To clarify the function of this protein, we have undertaken a genetic analysis of the synaptotagmin gene in Drosophila. We have identified five lethal alleles of synaptotagmin, at least one of which lacks detectable protein. Surprisingly, however, many embryos homozygous for this null allele hatch and, as larvae, crawl, feed, and respond to stimuli. Electrophysiological recordings in embryonic cultures confirmed that synaptic transmission persists in the null allele. Therefore, synaptotagmin is not absolutely required for the regulated exocytosis of synaptic vesicles. The lethality of synaptotagmin in late first instar larvae is probably due to a perturbation of transmission that leaves the main apparatus for vesicle docking and fusion intact.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Calcium-Binding Proteins*
  • DNA Mutational Analysis
  • Drosophila / metabolism*
  • Electrophysiology
  • Genes, Lethal
  • Membrane Glycoproteins / genetics*
  • Membrane Glycoproteins / metabolism
  • Nerve Tissue Proteins / genetics*
  • Nerve Tissue Proteins / metabolism
  • Neurotransmitter Agents / metabolism
  • Synaptic Vesicles / metabolism
  • Synaptotagmins

Substances

  • Calcium-Binding Proteins
  • Membrane Glycoproteins
  • Nerve Tissue Proteins
  • Neurotransmitter Agents
  • Synaptotagmins