|  Help  |  About  |  Contact Us

Publication : Neuron-specific gene expression of synapsin I. Major role of a negative regulatory mechanism.

First Author  Schoch S Year  1996
Journal  J Biol Chem Volume  271
Issue  6 Pages  3317-23
PubMed ID  8621737 Mgi Jnum  J:31353
Mgi Id  MGI:78855 Doi  10.1074/jbc.271.6.3317
Citation  Schoch S, et al. (1996) Neuron-specific gene expression of synapsin I. Major role of a negative regulatory mechanism. J Biol Chem 271(6):3317-23
abstractText  The synapsins are a family of neuron-specific phosphoproteins that selectively bind to small synaptic vesicles in the presynaptic nerve terminal. The human synapsin I gene was functionally analyzed to identify control elements directing the neuron-specific expression of synapsin I. By directly measuring the mRNA transcripts of a reporter gene, we demonstrate that the proximal region of the synapsin I promoter is sufficient for directing neuron-specific gene expression. This proximal region is highly conserved between mouse and human. Deletion of a putative binding site for the zinc finger protein, neuron-restrictive silencer factor/RE-1 silencing transcription factor (NRSF/REST), abolished neuron-specific expression of the reporter gene almost entirely, allowing constitutively acting elements of the promoter to direct expression in a non-tissue-specific manner. These constitutive transcriptional elements are present as a bipartite enhancer, consisting of the region upstream (nucleotides -422 to -235) and downstream (nucleotides -199 to -143) of the putative NRSF/REST-binding site. The latter contains a motif identical to the cAMP response element. Both regions are not active or are only weakly active in promoting transcription on their own and show no tissue-specific preference. From these data we conclude that neuron-specific expression of synapsin I is accomplished by a negative regulatory mechanism via the NRSF/REST binding motif.
Quick Links:
 
Quick Links:
 

Expression

Publication --> Expression annotations

 

Other

3 Authors

1 Bio Entities

Trail: Publication

0 Expression