Cloning and expression during development of three murine members of the COUP family of nuclear orphan receptors

Jonk, Luigi J.C.; Jonge, Marjolijn E.J. de; Pals, Cornelieke E.G.M.; Wissink, Sacha; Vervaart, Josée M.A.; Schoorlemmer, Jon; Kruijer, W.

doi:10.1016/0925-4773(94)90098-1

Cited by 138 publications

(122 citation statements)

References 48 publications

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“…In addition, COUP-TFI and COUP-TFII are highly conserved among different species, suggesting that they play important roles in development. Although the expression of COUP-TFI and COUP-TFII is highly overlapping in mice (24,43), COUP-TFI is abundantly expressed in the central and peripheral nervous system, while COUP-TFII is highly expressed in the mesenchymal component of the developing organs (46). Based on this expression pattern, we have proposed that COUP-TFI is important for neural development and that COUP-TFII is important in organogenesis through the regulation of mesenchymal cell-epithelial cell interactions.…”

mentioning

confidence: 98%

COUP-TF Upregulates NGFI-A Gene Expression through an Sp1 Binding Site

Pipaón

Tsai

1999

Molecular and Cellular Biology

109

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There are two COUP-TF genes, COUP-TFI and COUP-TFII (for a review, see reference 58), which share a high degree of homology in their DBDs and putative LBDs. In addition, COUP-TFI and COUP-TFII are highly conserved among different species, suggesting that they play important roles in development. Although the expression of COUP-TFI and COUP-TFII is highly overlapping in mice (24, 43), COUP-TFI is abundantly expressed in the central and peripheral nervous system, while COUP-TFII is highly expressed in the mesenchymal component of the developing organs (46). Based on this expression pattern, we have proposed that COUP-TFI is important for neural development and that COUP-TFII is important in organogenesis through the regulation of mesenchymal cell-epithelial cell interactions. Indeed, the targeted disruption of either of these two genes in mice results in a lethal phenotype. COUP-TFI-deficient mice show defects in the development of the central and peripheral nervous systems (47; unpublished observations), whereas mutation of the COUP-TFII gene results in defects in the heart and vasculature formation (unpublished observations).Vasculature and organ formation requires very tight communication between epithelial cell and mesenchymal cell populations (7). This communication is essential for the differentiation of these two cell types (14). Since COUP-TFII is highly expressed in the mesenchyme but is undetectable in the epithelium of most organs, it is likely that COUP-TFII plays an important role in mesenchymal cell-epithelial cell interactions during organogenesis. This process has been well studied for the prostate, where several growth factors and the extracellular matrix are involved in this communication between the mesenchyme and the epithelium (11,19).COUP-TFs are able to bind to a variety of dispositions of the basic AGGTCA motif, including those recognized by the receptors of retinoic acid (RAR), thyroid hormone, and vitamin D (13). This ability makes COUP-TFs capable of competing for the response elements of these receptors, thus acting as passive repressors of the transcriptional activation induced by them (12,13,56). Another mechanism of passive repression by COUP-TFs involves their ability to heterodimerize with the 9-cis retinoic acid receptor (RXR), reducing its availability for other nuclear receptors that use it as a partner. In addition, COUP-TFs contain an active repression domain within their putative LBDs (1,31). This repression domain is capable of interacting with corepressors such as SMRT and N-CoR (50), molecules that can recruit histone deacetylase activities to the DNA to suppress transcription (2,23,39).

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mentioning

confidence: 98%

COUP-TF Upregulates NGFI-A Gene Expression through an Sp1 Binding Site

Pipaón

Tsai

1999

Molecular and Cellular Biology

109

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“…This family includes receptors for sexual and adrenal steroids, retinoids, thyroid hormone, vitamin D, and ecdysone and a number of receptors whose ligands are still unknown and which are called orphan receptors (43,47). One of these orphan receptors, COUP-TF, is the most highly conserved member of the family, suggesting a conservation of COUP-TF functions from sea urchins to humans (5,11,12,22,30,45,46,68,69).…”

mentioning

confidence: 99%

The Nuclear Orphan Receptors COUP-TF and ARP-1 Positively Regulate the Trout Estrogen Receptor Gene through Enhancing Autoregulation

Lazennec

Kern

Valotaire

et al. 1997

Molecular and Cellular Biology

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The rainbow trout estrogen receptor (rtER) is a positively autoregulated gene in liver cells. In a previous report, we showed that upregulation is mediated by an estrogen response element (ERE) located in the proximal promoter of the gene and that a half binding site for nuclear receptors (5-TGACCT-3) located 15 bp upstream of the ERE is involved in the magnitude of the estrogen response. We now report that the human orphan receptor COUP-TF and a COUP-TF-like protein from trout liver are able to bind to the consensus half-site. When cotransfected with the rtER gene proximal promoter, COUP-TF had no regulatory functions on its own. Interestingly, COUP-TF enhanced rtER transactivation properties in the presence of estradiol in a dose-dependent manner when cotransfected with the rtER gene promoter. Unliganded retinoid receptor heterodimers had the same helper function as COUP-TF in the presence of estradiol but were switched to repressors when the ligand all-trans-retinoic acid was added. Mutation of the consensus half-site only slightly reduced COUP-TF helper function, suggesting that it actually results from a complex mechanism that probably involves both DNA binding of COUP-TF to the promoter and protein-protein interaction with another transcription factor bound to the promoter. Nevertheless, a DNA-binding-defective mutant of COUP-TF was also defective in ER helper function. Competition footprinting analysis suggested that COUP-TF actually establishes contacts with the consensus upstream half-site and the downstream ERE half-site that would form a DR-24-like response element. Interaction of COUP-TF with the DR-24 element was confirmed in footprinting assays by using nuclear extracts from Saccharomyces cerevisiae expressing COUP-TF. Finally, interaction of COUP-TF with mutants of the rtER gene promoter showed that COUP-TF recognizes the ERE when the upstream half-site is mutated. These data show that COUP-TF may activate transcription through interaction with other nuclear receptors. This cross-talk between liganded nuclear receptors and orphan receptors is likely to modulate the spectrum of action of a particular ligand-receptor complex and may participate in the cell-type specificity of the ligand effect.

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“…Expression-In addition to negatively regulating the expression of certain RA target genes, COUP-TFIs have themselves been demonstrated to be RA targets (12,22,23). This finding has led to the hypothesis that COUP-TFs are involved in a negative feedback mechanism that serves to repress the expression of RA target genes (23).…”

Section: Ra Induction Of Coup-tfi Leads To Down-regulation Of Cdx1mentioning

confidence: 99%

“…Chicken ovalbumin upstream promoter-transcription factors (COUP-TFI and COUP-TFII) are orphan nuclear receptors (11)(12)(13). COUP-TFs have been shown to interfere with many nuclear receptor signaling pathways including the RARs (14 -18).…”

Section: Cdx1mentioning

confidence: 99%

Chicken Ovalbumin Upstream Promoter-Transcription Factor Members Repress Retinoic Acid-induced Cdx1 Expression

Béland

Lohnes

2005

Journal of Biological Chemistry

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It is well established that Hox genes are key players in specifying positional identity along the anterior-posterior axis and are targets of diverse transcription factors implicated in axial patterning. Members of the CDX family (CDX1, -2, and -4) are among such effectors of Hox expression as pertains to vertebral patterning in the mouse. Cdx members are themselves targets of signaling molecules that are also implicated in axial patterning, including retinoic acid (RA) and certain members of Wnt and fibroblast growth factor families. In this regard, we have previously shown that, in the mouse, Cdx1 is directly regulated by RA at the late primitive streak stage (embryonic day (E) 7.5) through a RA response element in the proximal Cdx1 promoter. At E8.5, Cdx1 expression remains essentially limited to the posterior embryo. RA, however, is excluded from the caudal embryo at this later stage, but is found in a more anterior domain encompassing the prospective trunk region. These observations suggest the existence of a repressor mechanism that prevents expression of Cdx1 in these anterior domains of retinoid signaling at E8.5. In the present study, we present evidence suggesting that chicken ovalbumin upstream promoter-transcription factor (COUP-TF) members antagonize RA-induced Cdx1 expression by competing with retinoid X receptor-retinoic acid receptor heterodimers for binding to the Cdx1 RA response element. Consistent with this, in situ hybridization analysis revealed that COUP-TFs are highly expressed in the anterior embryo in domains where Cdx1 transcripts are excluded. Together with other data, these findings suggest a model by which COUP-TF expression is induced by RA in the trunk region as a negative feedback mechanism to restrict Cdx1 expression to the caudal embryo.

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Cloning and expression during development of three murine members of the COUP family of nuclear orphan receptors

Cited by 138 publications

References 48 publications

COUP-TF Upregulates NGFI-A Gene Expression through an Sp1 Binding Site

COUP-TF Upregulates NGFI-A Gene Expression through an Sp1 Binding Site

The Nuclear Orphan Receptors COUP-TF and ARP-1 Positively Regulate the Trout Estrogen Receptor Gene through Enhancing Autoregulation

Chicken Ovalbumin Upstream Promoter-Transcription Factor Members Repress Retinoic Acid-induced Cdx1 Expression

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