Mouse and human retinoic acid receptor β2 promoters: sequence comparison and localization of retinoic acid responsiveness

Shen, Sanbing; Fa, Kruyt; J, den Hertog; Saag, van der; Kruijer, W.

doi:10.3109/10425179109039679

Cited by 43 publications

(34 citation statements)

References 34 publications

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“…In this region we can identify nine HpaII sites (Shen et al, 1991;Baust et al, 1996). The DNA methylation status was analysed by using the methylation-sensitive enzyme, HpaII ( Figure 1b).…”

Section: Resultsmentioning

confidence: 99%

“…(Figure 1b). Using methylation-speci®c PCR (MSP), we further analysed a 616 bp long RARb2 region from nucleotide 481 to nucleotide 1096 (Shen et al, 1991) in all the cell lines. MSP entails the modi®cation of genomic DNA by sodium bisul®te that converts all unmethylated, but not methylated, cytosine to uracil (Herman et al, 1996).…”

Section: Resultsmentioning

confidence: 99%

“…Twelve ml of the PCR reaction were electrophoresed onto 1.5% agarose gels, stained with ethidium bromide and visualized under UV. Two primer pairs, W3 sense 5'-CAGCCCGGGTAGGGTTCACC-3', W3 antisense 5'-CCGGATCCTACCCCGACGG-3', and W4 sense 5'-CCGAGAACGCGAGCGATCC-3' and W4 antisense 5'-GGCCAATCCAGCCGGGGCG-3', were designed on the human RARb2 sequence (Shen et al, 1991) and used to control the Na bisul®te modi®cation. The primer pairs selected to detect the unmethylated DNA were as follows: U1 sense 5'-GTG GGT GTA GGT GGA ATA TT-3' and U1 antisense 5'-AAC AAA CAC ACA AAC CAA CA-3' (at 558C); U2 sense 5'-TGT GAG TTA GGA GTA GTG TTT T-3' and U2 antisense 5'-TTC AAT AAA CCC TAC CCA-3' (at 498C); U3 sense 5'-TTA GTA GTT TGG GTA GGG TTT ATT-3' and U3 antisense 5'-CCA AAT CCT ACC CCA ACA-3' (at 558C); U4 sense 5'-GAT GTT GAG AAT GTG AGT GAT TT-3' and U4 antisense 5'-AAC CAA TCC AAC CAA AAC A-3' (at 558C); The sequences of the primers to detect the methylated DNA were: M1 sense 5'-AGC GGG CGT AGG CGG AAT ATC-3' and M1 antisense 5'-CAA CGA ACG CAC AAA CCG ACG-3' (at 638C); M2 sense 5'-CGT GAG TTA GGA GTA GCG TTT C-3' and M2 antisense 5'-CTT TCG ATA AAC CCT ACC CG-3' (at 578C); M3 sense 5'-GGT TAG TAG TTC GGG TAG GGT TTA TC-3' and M3 antisense 5'-CCG AAT CCT ACC CCG ACG-3' (at 648C); M4 sense 5'-GTC GAG AAC GCG AGC GAT TC-3' and M4 antisense 5'-CGA CCA ATC CAA CCG AAA CG-3' (at 648C).…”

Section: Methylation Specific Pcr (Msp)mentioning

confidence: 99%

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Evidence of epigenetic changes affecting the chromatin state of the retinoic acid receptor β2 promoter in breast cancer cells

et al. 2000

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Section: Methylation Specific Pcr (Msp)mentioning

confidence: 99%

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Evidence of epigenetic changes affecting the chromatin state of the retinoic acid receptor β2 promoter in breast cancer cells

et al. 2000

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“…The nomenclature of RAR␤ isoforms is based on correlation to mouse and human RAR␤ isoforms. on May 12, 2018 by guest http://mcb.asm.org/ (10,11,47). To test the at-RA and TLX responsiveness of SET, we subcloned each element into a luciferase reporter driven by a tk minimal promoter.…”

Section: (42)mentioning

confidence: 99%

Cell-Type-Specific Regulation of the Retinoic Acid Receptor Mediated by the Orphan Nuclear Receptor TLX

Kobayashi

Yasuda

et al. 2000

Molecular and Cellular Biology

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Malformations in the eye can be caused by either an excess or deficiency of retinoids. An early target gene of the retinoid metabolite, retinoic acid (RA), is that encoding one of its own receptors, the retinoic acid receptor ␤ (RAR␤). To better understand the mechanisms underlying this autologous regulation, we characterized the chick RAR␤2 promoter. The region surrounding the transcription start site of the avian RAR␤2 promoter is over 90% conserved with the corresponding region in mammals and confers strong RA-dependent transactivation in primary cultured embryonic retina cells. This response is selective for RAR but not retinoid X receptor-specific agonists, demonstrating a principal role for RAR(s) in retina cells. Retina cells exhibit a far higher sensitivity to RA than do fibroblasts or osteoblasts, a property we found likely due to expression of the orphan nuclear receptor TLX. Ectopic expression of TLX in fibroblasts resulted in increased sensitivity to RA induction, an effect that is conserved between chick and mammals. We have identified a cis element, the silencing element relieved by TLX (SET), within the RAR␤2 promoter region which confers TLX-and RA-dependent transactivation. These results indicate an important role for TLX in autologous regulation of the RAR␤ gene in the eye.

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“…One of the immediate-early genes induced in P19 embryonal carcinoma (EC) cells by RA is the retinoic acid receptor ␤2 (RAR␤2) gene (49,64). The promoter region of this gene contains an RA responsive element (RARE) to which the nuclear hormone receptor heterodimer RAR-retinoid X receptor (RXR) binds (14,34).…”

mentioning

confidence: 99%

Retinoid-Induced Chromatin Structure Alterations in the Retinoic Acid Receptor β2 Promoter

Bhattacharyya

Dey

Minucci

et al. 1997

Molecular and Cellular Biology

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Transcription of the retinoic acid receptor ␤2 (RAR␤2) gene is induced by retinoic acid (RA) in mouse P19 embryonal carcinoma (EC) cells. Here we studied RA-induced chromatin structure alterations in the endogenous RAR␤2 promoter and in an integrated, multicopy RAR␤2 promoter in EC cells. RA markedly increased restriction site accessibility within the promoter, including a site near the RA responsive element (RARE) to which the nuclear receptor retinoid X receptor (RXR)-RAR heterodimer binds. These changes coincided with RA-induced alterations in the DNase I hypersensitivity pattern in and around the promoter. These changes became undetectable upon removal of RA, which coincided with the extinction of transcription. Analyses with receptor-selective ligands and an antagonist showed that increase in restriction site accessibility correlates with transcriptional activation, which parallels the RA-induced in vivo footprint of the promoter. Despite these changes, the micrococcal nuclease digestion profile of this promoter was not altered by RA. These results indicate that concurrent with the binding of the RXR-RAR heterodimer to the RARE, the local chromatin structure undergoes dynamic, reversible changes in and around the promoter without globally affecting the nucleosomal organization.It has been shown that retinoic acid (RA) induces expression of many genes in different cell types, while repressing expression of other genes (14, 34). One of the immediate-early genes induced in P19 embryonal carcinoma (EC) cells by RA is the retinoic acid receptor ␤2 (RAR␤2) gene (49, 64). The promoter region of this gene contains an RA responsive element (RARE) to which the nuclear hormone receptor heterodimer RAR-retinoid X receptor (RXR) binds (14, 34). Previous in vivo footprinting analyses showed that the RAR␤2 promoter is not occupied in P19 cells prior to RA addition, but after RA addition, occupancy is induced in the RARE and other cisacting elements that coincides with transcriptional activation of the promoter (7,17,37,38). Ligand-dependent occupancy of the RAR␤2 promoter has been recently confirmed by others in NB4 cells (16). In contrast, in vitro the RXR-RAR heterodimer can bind to the RARE in the absence of ligand. Binding of the heterodimer to DNA in vitro has been demonstrated even in the presence of corepressors, such as N-CoR, RIP13, and SMRT (15, 24). The striking differences observed between in vitro and in vivo studies suggest that accessibility of transcription factors to the promoter in vivo is governed by a mechanism that is not readily reconstituted in vitro and which may involve regulation by chromatin.It has been shown that chromatin structure plays an important role in gene activation (1,29,33,45,57,60). Several hormone-responsive promoters have been shown to undergo chromatin structure alterations following hormone addition.For example, a glucocorticoid-hormone-dependent alteration of nucleosomal positioning as well as a hormone-dependent DNase I hypersensitivity site has been observed for the rat tyros...

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Mouse and human retinoic acid receptor β2 promoters: sequence comparison and localization of retinoic acid responsiveness

Cited by 43 publications

References 34 publications

Evidence of epigenetic changes affecting the chromatin state of the retinoic acid receptor β2 promoter in breast cancer cells

Evidence of epigenetic changes affecting the chromatin state of the retinoic acid receptor β2 promoter in breast cancer cells

Cell-Type-Specific Regulation of the Retinoic Acid Receptor Mediated by the Orphan Nuclear Receptor TLX

Retinoid-Induced Chromatin Structure Alterations in the Retinoic Acid Receptor β2 Promoter

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