- page settings
- showhide sidebar
- showhide empty fields
- layout
- (too narrow)
- open all
- close all
- Page Content
- Overview
- External Links
- History
- Referenced
- Tools
- Tree Display
- My WormBase
- My Favorites
- My Library
- Recent Activity
- Comments (0)
history logging is off
Tree Display
My Favorites
My Library
Comments on Klosterman, Susan M. et al. (2013) International Worm Meeting "VPS-39 promotes synaptic vesicle fusion in C. elegans." (0)
Overview
Klosterman, Susan M., Yu, Szi-Chieh, Burdina, Anna O., & Richmond, Janet E. (2013). VPS-39 promotes synaptic vesicle fusion in C. elegans presented in International Worm Meeting. Unpublished information; cite only with author permission.
C. elegans tomosyn (TOM-1) negatively regulates synaptic transmission through interactions with syntaxin and SNAP-25, components of the core vesicle fusion machinery. In a yeast two-hybrid screen for TOM-1 binding partners, we identified an additional interactor, VPS-39, which is a highly conserved member of the HOPS (homotypic fusion and protein transport) complex. Since the HOPS complex has been implicated in the regulation of SNARE-dependent fusion, we obtained vps-39 mutants from the CGC to examine the potential role of this protein in synaptic vesicle exocytosis. Homozygous vps-39 mutants from a GFP balanced strain, grow to adulthood but lay dead embryos. A vps-39 translational mCherry fusion construct, capable of rescuing this embryonic lethality, indicates that VPS-39 is expressed in many tissues, including neurons. Furthermore, the vps-39 mutants exhibit pharmacological, electrophysiological and ultrastructural evidence of reduced neurotransmitter release. Both the lethality and synaptic defects of vps-39 mutants can be reversed by expressing VPS-39 specifically in neurons, indicating that these functions are cell autonomous. Epistasis experiments suggest that VPS-39 functions upstream of the priming factor, UNC-13. Experiments are presently underway to explore the relationship between VPS-39 and TOM-1 function in the synaptic vesicle cycle and further define which stage of the release process is impacted.
Affiliation:
- Dept Biol, Univ Illinois Chicago, Chicago, IL.