The retinoic acid receptor beta (RAR beta) gene is a member of the family of retinoic acid/thyroid hormone receptor genes, encoding retinoic acid-inducible transcription factors. To study regulation of the RAR beta gene, genomic clones containing the mouse and human retinoic acid receptor beta 2 (RAR beta 2) promoters were isolated and approximately 1.5 kb of upstream and downstream sequences relative to the transcriptional start site were completely sequenced. Both the mouse and human RAR beta 2 promoters are highly homologous around the transcription initiation site, with perfect conservation of the TATA box and retinoic acid responsive element (RARE). Promoter activation studies in P19 EC cells show, that the RARE in both the human and mouse promoters confers RA-responsiveness to the RAR beta 2 promoter. However, sequences located immediately upstream of the RARE also confer RA-inducibility to both the mouse and human RAR beta 2 gene promoters. This region contains conserved consensus sequences for a TPA-responsive element (TRE) and cAMP-responsive element (CRE), suggesting that in addition to regulation by RA receptors other transcription factors regulate RAR beta 2 expression in EC cells. Furthermore, the availability of the mouse RAR beta 2 promoter should facilitate studies for transgene expression and gene targeting experiments in embryonic stem cells.
SOURCE/DESCRIPTION: 1.4 kb Mae I fragment containing the entire RAR-, ORF cloned into the Sma I site of pTZ18U, yielding the plasmid pCOD20 (Brand et al., 1988). POLYMORPHISM: Msp I digestion of genomic DNA and hybridisation with the pCOD20 probe detects a two allele polymorphism with allelic fragments of 8.1 and 7.7 kb.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.