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Gene Review

nSyb  -  neuronal Synaptobrevin

Drosophila melanogaster

Synonyms: CG17248, Dmel\CG17248, Dn-syb, N-SYB, N-Syb, ...
 
 
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Disease relevance of n-syb

 

High impact information on n-syb

 

Biological context of n-syb

  • Expression of syb can restore synaptic transmission to n-syb mutants as assayed both by electroretinogram and recordings of excitatory junctional currents at the neuromuscular junction [4].
  • Mutant phenotypes and gene-expression patterns indicate that n-Syb is exclusively neuronal and required only for synaptic vesicle secretion, whereas Syb is ubiquitous and, as shown here, essential for cell viability [4].
  • Because of their distribution in the nervous system and because n-syb, synaptotagmin, and drab3 do not appear to be in a family of functionally redundant homologs, we predict that mutation of these genes will have a profound neurological phenotype and that they are therefore good candidates for a genetic dissection in Drosophila [6].
  • A neuronal Drosophila vamp (n-syb) is described here and is localized to chromosome band 62A [6].
  • Overexpression of Sp1, however, clearly activated transcription of a reporter gene under the control of the synaptobrevin II promoter (G+C)-rich sequence in Drosophila SL2 cells, which provided an Sp1-deficient background [7].
 

Anatomical context of n-syb

  • We suggest, using different membrane markers, that this apparent postsynaptic enrichment simply reflects a concentration of plasma membrane in the SSR, rather than a selective targeting of n-syb GFP to postsynaptic sites [8].
  • Surprisingly, n-syb GFP expressed in muscle is concentrated at the subsynaptic reticulum (SSR), postsynaptic infoldings of muscle plasma membrane [8].
  • Our results demonstrate the requirement of neuronal synaptobrevin for regulation of cell adhesion molecules and development of the fine structure of the optic lobe [9].
  • In genetic mosaics, patches of photoreceptors that lack neuronal synaptobrevin exhibit the same phenotypes observed after photoreceptor-specific toxin expression [9].
  • Neuropil pattern formation and regulation of cell adhesion molecules in Drosophila optic lobe development depend on synaptobrevin [9].
 

Associations of n-syb with chemical compounds

  • Furthermore, Ca(2+)-independent enhancement of mini frequency induced by hypertonic sucrose solutions (hypertonicity response) is totally absent in N-SYB [10].
  • Previously we reported that cAMP enhances spontaneous transmitter release in the absence of extracellular Ca(2+) and that the synaptic vesicle protein neuronal-synaptobrevin (n-syb), is required in this enhancement (n-syb-dependent; Yoshihara et al., 1999) [11].
  • The frequency of mSCs increased in response to elevation of cAMP, and this effect of cAMP was completely blocked by Co(2+) (n-syb-independent pathway) [11].
  • Three criteria were used to establish that other neuron-specific antigens--neuronal synaptobrevin and cysteine-string proteins--are legitimate components of synaptic vesicles: cosedimentation with Drosophila synaptotagmin, immunoadsorption, and disappearance of these antigens from the vesicle fractions in paralyzed shibire flies [12].
 

Regulatory relationships of n-syb

  • These vesicles are mature and functional since spontaneous vesicle fusion persists in the absence of n-synaptobrevin and since vesicle fusion is triggered by hyperosmotic saline in the absence of syntaxin [3].

References

  1. Targeted expression of tetanus toxin light chain in Drosophila specifically eliminates synaptic transmission and causes behavioral defects. Sweeney, S.T., Broadie, K., Keane, J., Niemann, H., O'Kane, C.J. Neuron (1995) [Pubmed]
  2. Drosophila UNC-13 is essential for synaptic transmission. Aravamudan, B., Fergestad, T., Davis, W.S., Rodesch, C.K., Broadie, K. Nat. Neurosci. (1999) [Pubmed]
  3. Syntaxin and synaptobrevin function downstream of vesicle docking in Drosophila. Broadie, K., Prokop, A., Bellen, H.J., O'Kane, C.J., Schulze, K.L., Sweeney, S.T. Neuron (1995) [Pubmed]
  4. Members of the synaptobrevin/vesicle-associated membrane protein (VAMP) family in Drosophila are functionally interchangeable in vivo for neurotransmitter release and cell viability. Bhattacharya, S., Stewart, B.A., Niemeyer, B.A., Burgess, R.W., McCabe, B.D., Lin, P., Boulianne, G., O'Kane, C.J., Schwarz, T.L. Proc. Natl. Acad. Sci. U.S.A. (2002) [Pubmed]
  5. Selective effects of neuronal-synaptobrevin mutations on transmitter release evoked by sustained versus transient Ca2+ increases and by cAMP. Yoshihara, M., Ueda, A., Zhang, D., Deitcher, D.L., Schwarz, T.L., Kidokoro, Y. J. Neurosci. (1999) [Pubmed]
  6. Identification and characterization of Drosophila genes for synaptic vesicle proteins. DiAntonio, A., Burgess, R.W., Chin, A.C., Deitcher, D.L., Scheller, R.H., Schwarz, T.L. J. Neurosci. (1993) [Pubmed]
  7. Role of zinc-finger proteins Sp1 and zif268/egr-1 in transcriptional regulation of the human synaptobrevin II gene. Petersohn, D., Thiel, G. Eur. J. Biochem. (1996) [Pubmed]
  8. Synaptic localization and restricted diffusion of a Drosophila neuronal synaptobrevin--green fluorescent protein chimera in vivo. Estes, P.S., Ho, G.L., Narayanan, R., Ramaswami, M. J. Neurogenet. (2000) [Pubmed]
  9. Neuropil pattern formation and regulation of cell adhesion molecules in Drosophila optic lobe development depend on synaptobrevin. Hiesinger, P.R., Reiter, C., Schau, H., Fischbach, K.F. J. Neurosci. (1999) [Pubmed]
  10. Roles of SNARE proteins and synaptotagmin I in synaptic transmission: studies at the Drosophila neuromuscular synapse. Kidokoro, Y. Neurosignals (2003) [Pubmed]
  11. Two independent pathways mediated by cAMP and protein kinase A enhance spontaneous transmitter release at Drosophila neuromuscular junctions. Yoshihara, M., Suzuki, K., Kidokoro, Y. J. Neurosci. (2000) [Pubmed]
  12. Redistribution of synaptic vesicles and their proteins in temperature-sensitive shibire(ts1) mutant Drosophila. van de Goor, J., Ramaswami, M., Kelly, R. Proc. Natl. Acad. Sci. U.S.A. (1995) [Pubmed]
 
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