The bidirectional promoter of the divergently transcribed mouse Surf-1 and Surf-2 genes.

Lennard, Andrew; Fried, Mike

doi:10.1128/mcb.11.3.1281

Cited by 61 publications

(39 citation statements)

References 37 publications

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“…1B). Similar genomic structures have been seen in many other gene systems (8)(9)(10)(11)(12)(13). In addition, a plasmid containing a TL and HEPH gene and the ,BGAP motif has been shown to express both genes after being transfected into various cell lines (7).…”

Section: Resultsmentioning

confidence: 60%

beta2 knockout mice develop parenchymal iron overload: A putative role for class I genes of the major histocompatibility complex in iron metabolism.

Rothenberg

Voland

1996

Proc. Natl. Acad. Sci. U.S.A.

184

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Hemochromatosis (HC) is an inherited disorder of iron absorption, mapping within the human major histocompatibility complex (MHC). We have identified a multigene system in the murine MHC that contains excellent candidates for the murine equivalent of the human HC locus and implicate nonclassical class I genes in the control of iron absorption. This gene system is characterized by multiple copies of two head-to-head genes encoded on opposite strands and driven by one common regulatory motif. This regulatory motif has a striking homology to the promoter region of the g3-globin gene, a gene obviously involved in iron metabolism and hence termed j8-globin analogous promoter (j3GAP).Upstream of the i3GAP sequence are nonclassical class I genes. At least one of these nonclassical class I genes, Q2, is expressed in the gastrointestinal tract, the primary site of iron absorption. Also expressed in the gastrointestinal tract and downstream of the .8GAP motif is a second set of putative genes, termed Hephaestus (HEPH). Based on these observations, we hypothesized that the genes that seem to be controlled by the 3GAP regulatory motifs would be responsible for the control of Fe absorption. As a test of this hypothesis, we predicted that mice which have altered expression of class I gene products, the 32-microglobulin knockout mice, [f32m(-/-)], would develop Fe overload. This prediction was confirmed, and these results indicate .32m-associated proteins are involved in the control of intestinal Fe absorption.

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Section: Resultsmentioning

confidence: 60%

beta2 knockout mice develop parenchymal iron overload: A putative role for class I genes of the major histocompatibility complex in iron metabolism.

Rothenberg

Voland

1996

Proc. Natl. Acad. Sci. U.S.A.

184

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“…The proximity and orientation of the GSTT2 and DDCT genes suggests that they may be under the control of a bidirectional promoter, such as those shown to occur within the mouse Surfeit locus [34,35]. The Surf genes are a closely linked cluster of unrelated genes that are arranged in head-to-head pairs.…”

Section: Discussionmentioning

confidence: 99%

Structure and organization of the human Theta-class glutathione S-transferase and d-dopachrome tautomerase gene complex

Coggan

Whitbread

Whittington

et al. 1998

Biochemical Journal

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The structure and organization of the human Theta-class glutathione S-transferase (GST) genes have been determined. GSTT1 and GSTT2 are separated by approx. 50 kb. They have a similar structure, being composed of five exons with identical exon/intron boundaries. GSTT1 is 8.1 kb in length, while GSTT2 is only 3.7 kb. The GSTT2 gene lies head-to-head with a gene encoding d-dopachrome tautomerase (DDCT), which extends over 8.5 kb and contains four exons. The sequence between GSTT2 and DDCT may contain a bidirectional promoter. The GSTT2 and DDCT genes have been duplicated in an inverted repeat. Sequence analysis of the duplicated GSTT2 gene has identified an exon 2/intron 2 splice site abnormality and a premature translation stop signal at codon 196. These changes suggest that the duplicate gene is a pseudogene, and it has been named GSTT2P.

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“…Ectopic expression of members of other families of bHLH proteins can also stimulate transcription through the USF recognition motif (3,5,39), clouding the understanding of how the various families of bHLH proteins work in vivo. Whether USF can function in a bidirectional manner was also unclear; some reports suggest that such a capacity exists (13,42,43), while others contend that USF cannot operate in this fashion (2). USF was not found to stimulate transcriptionally divergent promoters in a symmetrical fashion.…”

Section: Discussionmentioning

confidence: 99%

The cellular transcription factor USF cooperates with varicella-zoster virus immediate-early protein 62 to symmetrically activate a bidirectional viral promoter.

Meier¹,

Luo²,

Sawadogo³

et al. 1994

Mol. Cell. Biol.

100

109

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The mechanisms governing the function of cellular USF and herpesvirus immediate-early transcription factors are subjects of considerable interest. In this regard, we identified a novel form of coordinate gene regulation involving a cooperative interplay between cellular USF and the varicella-zoster virus immediateearly protein 62 (IE 62). A single USF-binding site defines the potential level of IE 62-dependent activation of a bidirectional viral early promoter of the DNA polymerase and major DNA-binding protein genes. We also report a dominant negative USF-2 mutant lacking the DNA-binding domain that permits the delineation of the biological role of both USF-1 and USF-2 in this activation process. The symmetrical stimulation of the bidirectional viral promoter by IE 62 is achieved at concentrations of USF-1 (43 kDa) or USF-2 (44 kDa) already existing in cells. Our observations support the notion that cellular USF can intervene in and possibly target promoters for activation by a herpesvirus immediate-early protein.

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The bidirectional promoter of the divergently transcribed mouse Surf-1 and Surf-2 genes.

Cited by 61 publications

References 37 publications

beta2 knockout mice develop parenchymal iron overload: A putative role for class I genes of the major histocompatibility complex in iron metabolism.

beta2 knockout mice develop parenchymal iron overload: A putative role for class I genes of the major histocompatibility complex in iron metabolism.

Structure and organization of the human Theta-class glutathione S-transferase and d-dopachrome tautomerase gene complex

The cellular transcription factor USF cooperates with varicella-zoster virus immediate-early protein 62 to symmetrically activate a bidirectional viral promoter.

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