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Published 28 April 2003. doi:10.1083/jcb.200211117
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© 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.


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