Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Evidence for a functional link between Rab3 and the SNARE complex

L Johannes1, F Doussau, A Clabecq

  • 1Service de Neurobiologie Physico-Chimique, Centre National de la Recherche Scientifique, UPR 9071, Institut de Biologie Physico-Chimique, Paris, France.

Journal of Cell Science
|December 1, 1996
PubMed
Summary
This summary is machine-generated.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

The experiences of pediatric nurses deployed to adult COVID-19 wards.

Archives de pediatrie : organe officiel de la Societe francaise de pediatrie·2023
Same author

Residency training in robotic surgery: The role of simulation.

Journal of visceral surgery·2020
Same author

Inhibition promotes long-term potentiation at cerebellar excitatory synapses.

Scientific reports·2016
Same author

Membrane invagination induced by Shiga toxin B-subunit: from molecular structure to tube formation.

Soft matter·2016
Same author

The role of oxidative damage in poor scalp health: ramifications to causality and associated hair growth.

International journal of cosmetic science·2015
Same author

Retrograde Trafficking Inhibitor of Shiga Toxins Reduces Morbidity and Mortality of Mice Infected with Enterohemorrhagic Escherichia coli.

Antimicrobial agents and chemotherapy·2015

Rab3 GTPase-deficient mutant protein inhibits acetylcholine release in Aplysia neurons, suggesting GTP hydrolysis is rate-limiting. This indicates Rab3 controls SNARE complex formation or stability in regulated exocytosis.

Area of Science:

  • Neuroscience
  • Cell Biology
  • Molecular Biology

Background:

  • Rab3 is a GTP-binding protein crucial for regulated exocytosis.
  • Its precise role in neurotransmitter release remains under investigation.

Purpose of the Study:

  • To investigate the function of Rab3 in neurotransmitter release using mutant proteins in Aplysia neurons.
  • To determine the specific step in the exocytosis process where Rab3 exerts its control.

Main Methods:

  • Utilized GTPase-deficient Rab3 mutant proteins in Aplysia neurons.
  • Applied tetanus and botulinum type A neurotoxins to cleave SNARE complex components (VAMP/synaptobrevin and SNAP-25).
  • Assessed the impact of mutant Rab3 on toxin-induced inhibition of neurotransmitter release.

Related Experiment Videos

Main Results:

  • A GTPase-deficient Rab3 mutant inhibited acetylcholine release, indicating GTP hydrolysis is rate-limiting.
  • This inhibitory effect was dependent on Rab3's effector domain and membrane association.
  • Neurotoxin-induced inhibition of release was delayed, suggesting mutant Rab3 accumulated a toxin-insensitive release component.

Conclusions:

  • Rab3 likely modulates the exocytosis machinery by regulating SNARE complex formation or stability.
  • GTP hydrolysis by Rab3 appears to be a rate-limiting step in regulated exocytosis.
  • Rab3's function is essential for proper neurotransmitter release control.