A common silencer element in the SCG10 and type II Na^+ channel genes binds a factor present in nonneuronal cells but not in neuronal cells
Abstract
We have localized a cell type-specific silencer element in the SCG10 gene by deletion analysis. This neural-restrictive silencer element (NRSE) selectively represses SCG10 expression in nonneuronal cells and tissues. The NRSE contains a 21 by region with striking homology to a sequence present in a silencer domain of the rat type II sodium channel (Nall), another neuron-specific gene. We have identified a sequence-specific protein(s) that binds the SCG10 NRSE, as well as the homologous element in the Nall gene. A point mutation in the NRSE that abolishes binding of this neural-restrictive silencerbinding factor (NRSBF) in vitro also eliminates silencing activity in vivo. NRSBF is present in nuclear extracts from nonneuronal cells but not in extracts from neuronal cells, suggesting that the neuron-specific expression of SCG10 reflects, at least in part, the absence or inactivity of this protein. These data identify the NRSE as a potentially general DNA element for the control of neuron-specific gene expression in vertebrates.
Additional Information
© 1992 Cell Press. Received March 6, 1992; Revised April 22, 1992. We are grateful to Dr. Carl Parker for his advice and the use of his facilities for growing large scale HeLa cell cultures and preparing nuclear extracts. We thank Dr. Takashi Okazaki for assistance with some of the transfection experiments, Steven Padilla for plasmid preparations, and Dr. Susan Birren, Dr. Barbara Wold, and one of the reviewers for their helpful comments on the manuscript. This work was supported by National Institutes of Health grant NS23476. D. J. A. is an Assistant Investigator of the Howard Hughes Medical Institute. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 USC Section 1734 solely to indicate this fact.Additional details
- Eprint ID
- 55152
- DOI
- 10.1016/0896-6273(92)90219-4
- Resolver ID
- CaltechAUTHORS:20150224-125023165
- NS23476
- NIH
- Howard Hughes Medical Institute (HHMI)
- Created
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2015-02-24Created from EPrint's datestamp field
- Updated
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2021-11-10Created from EPrint's last_modified field