JCB logo
Accuri Cytometers
  Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents
Published 28 April 2003. doi:10.1083/jcb.200211117
This Article
Right arrow Full Text
Right arrow Full Text (PDF, 77K)
Right arrow Alert me when this article is cited
Right arrow Citation Map
Services
Right arrow Email this article
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new content in the JCB
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via CrossRef
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Weston, A. D.
Right arrow Articles by Underhill, T. M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Weston, A. D.
Right arrow Articles by Underhill, T. M.
Social Bookmarking
Add to CiteULike   Add to Complore   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Reddit   Add to Technorati  
What's this?
© The Rockefeller University Press, 0021-9525/2003/4/223 $5.00
The Journal of Cell Biology, Volume 161, Number 2, 223-228

Mini-Review

 Active repression by unliganded retinoid receptors in development : less is sometimes more



Andrea D. Weston1, Bruce Blumberg2 and T. Michael Underhill3

1 Institute for Systems Biology, Seattle, WA 98103
2 Department of Developmental and Cell Biology, University of California, Irvine, CA 92697
3 Department of Physiology, Faculty of Medicine & Dentistry, The University of Western Ontario, London, Ontario, Canada N6A 5C1

Address correspondence to Andrea D. Weston, Institute for Systems Biology, 1441 N. 34th St., Seattle, WA 98103. Tel.: (206) 732-1381. Fax: (206) 732-1299. E-mail: aweston{at}systemsbiology.org

The retinoid receptors have major roles throughout development, even in the absence of ligand. Here, we summarize an emerging theme whereby gene repression, mediated by unliganded retinoid receptors, can dictate cell fate. In addition to activating transcription, retinoid receptors actively repress gene transcription by recruiting cofactors that promote chromatin compaction. Two developmental processes for which gene silencing by the retinoid receptors is essential are head formation in Xenopus and skeletal development in the mouse. Inappropriate repression, by oncogenic retinoic acid (RA)* receptor (RAR) fusion proteins, blocks myeloid differentiation leading to a rare form of leukemia. Our current understanding of the developmental role of retinoid repression and future perspectives in this field are discussed.

Key Words: cell differentiation; nuclear receptors; cofactors; chromatin remodeling; retinoid signaling

* Abbreviations used in this paper: APL, acute promyelocytic leukemia; dnRAR{alpha}, dominant–negative version of the RAR{alpha}; E, embryonic age; HDAC, histone deacetylase; LCoR, ligand-dependent corepressor; NCoR, nuclear receptor corepressor; RA, retinoic acid; RAR, RA receptor; RARE, RXR homodimer bound to bipartite response element; RXR, retinoid X receptor; TSA, trichostatin A; CYP26, cytochrome p450, 26; TR, thyroid hormone receptor.


Add to CiteULike CiteULike   Add to Complore Complore   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati    What's this?


This article has been cited by other articles:



  Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents