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This version published online on October 3, 2002
Molecular Endocrinology, doi:10.1210/me.2002-0192
A more recent version of this article appeared on January 1, 2003
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Submitted on May 23, 2002
Accepted on September 17, 2002

TRAPPING AND CHARACTERIZATION OF NOVEL RETINOID RESPONSE ELEMENTS

Michele A. Glozak1, Yong Li1, Rae Reuille1, Kwan Hee Kim1, My-Nuong Vo1, and Melissa B. Rogers1*

1 Biology and Institute for Biomolecular Science, University of South Florida, Tampa, FL, Genetics, Cell Biology, and Biochemistry, Washington State University, Pullman, WA, Biochemistry and Molecular Biology, UMDNJ-New Jersey Medical School, Newark, NJ, These authors contributed equally to this work.

* To whom correspondence should be addressed. E-mail: rogersmb{at}umdnj.edu,.

Retinoids, such as retinoic acid (RA), play a critical role in normal vertebrate development and physiology. However, embryonic exposure to excess retinoids also causes severe malformations. Retinoids bind retinoic acid receptors (RARs) and retinoid X receptors (RXRs) thus activating a plethora of genes. Separating the genes induced directly by retinoid bound receptors from those induced subsequently by other transcription factors is difficult. The loose consensus defining known retinoic acid responsive elements (RAREs) further complicates this effort. We developed a yeast-based system to trap functional RAREs in the mouse genome. Several of the clones contain RAREs near RA-induced genes. Mammalian reporter gene analyses and electrophoretic mobility shift assays showed that these are bona fide RAREs. This functional genomics approach should identify RA-regulated genes that initiate critical signaling cascades in cells.
Key words: Retinoic Acid (RA) • Retinoic Acid Response Element (RARE) • Retinoic Acid Receptor (RAR) • Retinoid X Receptor (RXR) • Saccharomyces cerevisiae • functional genomics • enhancer traps

NURSA Molecule Pages Link:

Nuclear Receptors:   RARβ  |  RXRγ
Ligands:   all-trans-Retinoic acid  |  9-cis-Retinoic acid



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