aex-3 encodes a novel regulator of presynaptic activity in C. elegans

Neuron. 1997 Apr;18(4):613-22. doi: 10.1016/s0896-6273(00)80302-5.


C. elegans aex-3 mutations cause pleiotropic behavioral defects that are suggestive of reduced synaptic transmission. aex-3 mutations also show strong genetic interactions with mutations in unc-31 and unc-64, two other genes implicated in synaptic transmission. Physiological and pharmacological studies indicate that aex-3 defects are presynaptic. In aex-3 mutants, the synaptic vesicle-associated RAB-3 protein aberrantly accumulates in neuronal cell bodies and is reduced in synapse-rich axons. This localization defect is specific to RAB-3, since other synaptic proteins are localized normally in aex-3 mutants. aex-3 encodes a 1409 amino acid protein with strong homology to DENN, a human protein of unknown function. In C. elegans, aex-3 is expressed in all or nearly all neurons. These results suggest that AEX-3 is a novel regulator of presynaptic activity that interacts with RAB-3 to regulate synaptic vesicle release.

Publication types

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

MeSH terms

  • Aldicarb / pharmacology
  • Amino Acid Sequence
  • Animals
  • Behavior, Animal / physiology
  • Caenorhabditis elegans / genetics*
  • Cholinesterase Inhibitors / pharmacology
  • Chromosome Mapping
  • Electrophysiology
  • GTP-Binding Proteins / metabolism
  • Genes*
  • Molecular Sequence Data
  • Mutation*
  • Nervous System Physiological Phenomena
  • Pharynx / innervation
  • Presynaptic Terminals / physiology*
  • Synapses / physiology
  • Synaptic Transmission
  • Tissue Distribution
  • rab3 GTP-Binding Proteins


  • Cholinesterase Inhibitors
  • Aldicarb
  • GTP-Binding Proteins
  • rab3 GTP-Binding Proteins