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Cited by 416

Corepressor-Dependent Silencing of Chromosomal Regions Encoding Neuronal Genes

Lunyak, Victoria V., Burgess, Robert, Prefontaine, Gratien G., Nelson, Charles, Sze, Sing-Hoi, Chenoweth, Josh, Schwartz, Phillip, Pevzner, Pavel A. +3 more·2002·Science
DOI 10.1126/science.1076469
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Abstract

The molecular mechanisms by which central nervous system–specific genes are expressed only in the nervous system and repressed in other tissues remain a central issue in developmental and regulatory biology. Here, we report that the zinc-finger gene-specific repressor element RE-1 silencing transcription factor/neuronal restricted silencing factor (REST/NRSF) can mediate extraneuronal restriction by imposing either active repression via histone deacetylase recruitment or long-term gene silencing using a distinct functional complex. Silencing of neuronal-specific genes requires the recruitment of an associated corepressor, CoREST, that serves as a functional molecular beacon for the recruitment of molecular machinery that imposes silencing across a chromosomal interval, including transcriptional units that do not themselves contain REST/NRSF response elements.

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Crossref · 10.1126/science.1076469

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4 of 4 references verified0 citation errors · 0 not checkable

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  • One putative mechanism underlying the transcriptional changes in Huntington's disease is aberrant cellular distribution of the transcriptional repressor REST.

    “One putative mechanism underlying the transcriptional changes is aberrant cellular distribution of the transcriptional repressor RE1-silencing transcription factor (REST, also known as neuronal restrictive silencing factor, NRSF) (Lunyak et al., 2002; Zuccato et al., 2003 ; Zuccato et al., 2007).”

    From The Bifunctional microRNA miR-9/miR-9* Regulates REST and CoREST and Is Downregulated in Huntington's Disease (2008) · cites this paper as Lunyak et al., 2002

  • miR-132 has been shown to target MeCP2, which can interact with REST and CoREST to suppress transcription.

    “MiR-132 has been shown to target MeCP2 (Klein et al., 2007), which can interact with REST and CoREST to suppress transcription (Lunyak et al., 2002).”

    From The Bifunctional microRNA miR-9/miR-9* Regulates REST and CoREST and Is Downregulated in Huntington's Disease (2008) · cites this paper as Lunyak et al., 2002

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Authors
Lunyak, V. V., Burgess, R., Prefontaine, G. G., Nelson, C., Sze, S.-H., Chenoweth, J., Schwartz, P., Pevzner, P. A., Glass, C., Mandel, G., & Rosenfeld, M. G.
Affiliations
  • Howard Hughes Medical Institute (HHMI),
  • Department of Computer Science and Engineering, School of Medicine, University of California, San Diego, 9500 Gilman Drive, Room 345, La Jolla, CA 92093–0648, USA.
  • Howard Hughes Medical Institute, Department of Neurobiology, State University of New York, Stony Brook, NY 11794, USA.
  • Affinity BioReagents, Incorporated, 14818 West 6th Avenue, Suite 10A, Golden, CO 80401, USA.
  • Department of Cellular and Molecular Medicine, School of Medicine, University of California, San Diego, La Jolla, CA 92093, USA.
Venue
Science
Publisher
American Association for the Advancement of Science (AAAS)
Published
2002-11-29
Volume
298
Issue
5599
Pages
1747-1752
ISSN
  • 0036-8075
  • 1095-9203
DOI
10.1126/science.1076469
Cited by
416
References
4
Language
en

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