A novel myoblast enhancer element mediates MyoD transcription

1992 ◽  
Vol 12 (11) ◽  
pp. 4994-5003
Author(s):  
S J Tapscott ◽  
A B Lassar ◽  
H Weintraub
Keyword(s):  
Skeletal Muscle ◽  
Specific Activity ◽  
Leukemia Virus ◽  
Regulatory Region ◽  
Simian Virus 40 ◽  
Simian Virus ◽  
Enhancer Element ◽  
Distal Regulatory Region ◽  
Avian Muscle ◽  
Moloney Leukemia Virus

The MyoD gene can orchestrate the expression of the skeletal muscle differentiation program. We have identified the regions of the gene necessary to reproduce transcription specific to skeletal myoblasts and myotubes. A proximal regulatory region (PRR) contains a conserved TATA box, a CCAAT box, and a GC-rich region that includes a consensus SP1 binding site. The PRR is sufficient for high levels of skeletal muscle-specific activity in avian muscle cells. In murine cells the PRR alone has only low levels of activity and requires an additional distal regulatory region to achieve high levels of muscle-specific activity. The distal regulatory region differs from a conventional enhancer in that chromosomal integration appears necessary for productive interactions with the PRR. While the Moloney leukemia virus long terminal repeat can enhance transcription from the MyoD PRR in both transient and stable assays, the simian virus 40 enhancer cannot, suggesting that specific enhancer-promoter interactions are necessary for PRR function.

scholarly journals A novel myoblast enhancer element mediates MyoD transcription.

1992 ◽  
Vol 12 (11) ◽  
pp. 4994-5003 ◽  
Author(s):  
S J Tapscott ◽  
A B Lassar ◽  
H Weintraub
Keyword(s):  
Skeletal Muscle ◽  
Specific Activity ◽  
Leukemia Virus ◽  
Regulatory Region ◽  
Simian Virus 40 ◽  
Simian Virus ◽  
Enhancer Element ◽  
Distal Regulatory Region ◽  
Avian Muscle ◽  
Moloney Leukemia Virus

The MyoD gene can orchestrate the expression of the skeletal muscle differentiation program. We have identified the regions of the gene necessary to reproduce transcription specific to skeletal myoblasts and myotubes. A proximal regulatory region (PRR) contains a conserved TATA box, a CCAAT box, and a GC-rich region that includes a consensus SP1 binding site. The PRR is sufficient for high levels of skeletal muscle-specific activity in avian muscle cells. In murine cells the PRR alone has only low levels of activity and requires an additional distal regulatory region to achieve high levels of muscle-specific activity. The distal regulatory region differs from a conventional enhancer in that chromosomal integration appears necessary for productive interactions with the PRR. While the Moloney leukemia virus long terminal repeat can enhance transcription from the MyoD PRR in both transient and stable assays, the simian virus 40 enhancer cannot, suggesting that specific enhancer-promoter interactions are necessary for PRR function.

Locations of nucleosomes on the regulatory region of simian virus 40 chromatin

1989 ◽  
Vol 210 (2) ◽  
pp. 255-263 ◽  
Author(s):  
Christine Ambrose ◽  
Anjali Rajadhyaksha ◽  
Henry Lowman ◽  
Minou Bina
Keyword(s):  
Regulatory Region ◽  
Simian Virus 40 ◽  
Simian Virus

Dynamics of the Nucleoprotein Structure of Simian Virus 40 Regulatory Region During Viral Development

1994 ◽  
Vol 238 (4) ◽  
pp. 501-513 ◽  
Author(s):  
Ariella Oppenheim ◽  
Merav Siani ◽  
Ziv Sandalon ◽  
Galina Mengeritsky
Keyword(s):  
Regulatory Region ◽  
Simian Virus 40 ◽  
Simian Virus ◽  
Viral Development

SR alpha promoter: an efficient and versatile mammalian cDNA expression system composed of the simian virus 40 early promoter and the R-U5 segment of human T-cell leukemia virus type 1 long terminal repeat

1988 ◽  
Vol 8 (1) ◽  
pp. 466-472 ◽  
Author(s):  
Y Takebe ◽  
M Seiki ◽  
J Fujisawa ◽  
P Hoy ◽  
K Yokota ◽  
...  
Keyword(s):  
Leukemia Virus ◽  
Expression System ◽  
Simian Virus 40 ◽  
Simian Virus ◽  
Cell Leukemia ◽  
Cell Leukemia Virus Type ◽  
Early Promoter ◽  
Human T Cell ◽  
T Cell Leukemia Virus

We developed a novel promoter system, designated SR alpha, which is composed of the simian virus 40 (SV40) early promoter and the R segment and part of the U5 sequence (R-U5') of the long terminal repeat of human T-cell leukemia virus type 1. The R-U5' sequence stimulated chloramphenicol acetyltransferase (CAT) gene expression only when placed immediately downstream of the SV40 early promoter in the sense orientation. The SR alpha expression system was 1 or 2 orders of magnitude more active than the SV40 early promoter in a wide variety of cell types, including fibroblasts and lymphoid cells, and was capable of promoting a high level of expression of various lymphokine cDNAs. These features of the SR alpha promoter were incorporated into the pcD-cDNA expression cloning vector originally developed by Okayama and Berg.

Lymphoid and other tissue-specific phenotypes of polyomavirus enhancer recombinants: positive and negative combinational effects on enhancer specificity and activity

1986 ◽  
Vol 6 (6) ◽  
pp. 2068-2079
Author(s):  
B A Campbell ◽  
L P Villarreal
Keyword(s):  
Cell Lines ◽  
Heavy Chain ◽  
Murine Leukemia Virus ◽  
Tissue Specificity ◽  
Leukemia Virus ◽  
Simian Virus 40 ◽  
Simian Virus ◽  
Lymphoid Cells ◽  
B Lymphoid ◽  
Murine Leukemia

Heterologous enhancer recombinants and deletions of the polyomavirus (Py) noncoding region were constructed and analyzed for tissue specificity of DNA replication and transcription in a number of lymphoid and other cell lines. The simian virus 40 72-base-pair repeat, mouse immunoglobulin heavy-chain enhancer, and Moloney murine leukemia virus enhancer were inserted into the PvuII-D locus (nucleotides 5128 through 5265) of Py. The ability of these recombinants and the parental PvuII-D deletion mutant to replicate in permissive 3T6 cells and MOP-6 cells as well as in nonpermissive mouse B lymphoid, T lymphoid, mastocyte, and embryonal carcinoma cells was determined. Wild-type Py DNA was not permissive for replication in most lymphoid cell lines, except one hybridoma line. Simply deleting the Py PvuII-D region, however, gave Py an expanded host range, allowing high-level replication in some T lymphoid and mastocytoma cell lines, indicating that this element can be a tissue-specific negative as well as positive element. Substitution of the murine leukemia virus enhancer for Py PvuII-D yielded a Py genome which retained the ability to replicate in 3T6 cells but also replicated well in B lymphoid cells. Substitution with the immunoglobulin heavy-chain enhancer allowed replication in B lymphoid cells but interfered with replication in 3T6 cells and mastocytomas. Surprisingly, substitution with the simian virus 40 72-base-pair enhancer repeat gave a recombinant which would not replicate in any cell line tried, including MOP-6 cells, even though other recombinants with this enhancer would replicate. Thus, we observed both cooperation and interference in these combinations between enhancer components and the Py genome and that these combined activities were cell specific. These results are presented as evidence that there may be a positional dependence, or syntax, for the recognition of genetic elements controlling Py tissue specificity.

scholarly journals trans-activation of the simian virus 40 enhancer by a pX product of human T-cell leukemia virus type I.

1988 ◽  
Vol 62 (2) ◽  
pp. 644-648 ◽  
Author(s):  
S Saito ◽  
M Nakamura ◽  
K Ohtani ◽  
M Ichijo ◽  
K Sugamura ◽  
...  
Keyword(s):  
T Cell ◽  
Virus Type ◽  
Leukemia Virus ◽  
Simian Virus 40 ◽  
Simian Virus ◽  
Type I ◽  
Cell Leukemia ◽  
Cell Leukemia Virus Type ◽  
Human T Cell ◽  
T Cell Leukemia Virus

Circular and linear simian virus 40 DNAs differ in recombination

1985 ◽  
Vol 5 (4) ◽  
pp. 869-880
Author(s):  
D Dorsett ◽  
I Deichaite ◽  
E Winocour
Keyword(s):  
Dna Sequences ◽  
Tandem Repeats ◽  
Regulatory Region ◽  
Simian Virus 40 ◽  
Simian Virus ◽  
T Antigen ◽  
Linear Forms ◽  
Rolling Circle ◽  
Linear Dna ◽  
Sv40 Dna

Linear forms of simian virus 40 (SV40) DNA, when added to transfection mixtures containing circular SV40 and phi X174 RFI DNAs, enhanced the frequency of SV40/phi X174 recombination, as measured by infectious center in situ plaque hybridization in monkey BSC-1 cells. The sequences required for the enhancement of recombination by linear DNA reside within the SV40 replication origin/regulatory region (nucleotides 5,171 to 5,243/0 to 128). Linearization of phi X174 RFI DNA did not increase the recombination frequency. The SV40/phi X174 recombinant structures arising from transfections supplemented with linear forms of origin-containing SV40 DNA contained phi X174 DNA sequences interspersed within tandem head-to-tail repeats derived from the recombination-enhancing linear DNA. Evidence is presented that the tandem repeats are not formed by homologous recombination and that linear forms of SV40 DNA must compete with circular SV40 DNA for the available T antigen to enhance recombination. We propose that the enhancement of recombination by linear SV40 DNA results from the entry of that DNA into a rolling circle type of replication pathway which generates highly recombinogenic intermediates.

scholarly journals Human mesotheliomas contain the simian virus-40 regulatory region and large tumor antigen DNA sequences

1998 ◽  
Vol 116 (5) ◽  
pp. 854-859 ◽  
Author(s):  
Harvey I. Pass ◽  
Jessica S. Donington ◽  
Peter Wu ◽  
Paola Rizzo ◽  
Michael Nishimura ◽  
...  
Keyword(s):  
Dna Sequences ◽  
Tumor Antigen ◽  
Regulatory Region ◽  
Simian Virus 40 ◽  
Simian Virus ◽  
Large Tumor ◽  
Large Tumor Antigen

scholarly journals A Genome-Wide Screen for β-Catenin Binding Sites Identifies a Downstream Enhancer Element That Controls c-Myc Gene Expression

2008 ◽  
Vol 28 (24) ◽  
pp. 7368-7379 ◽  
Author(s):  
Gregory S. Yochum ◽  
Ryan Cleland ◽  
Richard H. Goodman
Keyword(s):  
Binding Sites ◽  
Wnt Signaling Pathway ◽  
Simian Virus 40 ◽  
Simian Virus ◽  
Colorectal Carcinogenesis ◽  
Enhancer Element ◽  
Cancer Pathogenesis ◽  
Genome Wide ◽  
A Genome ◽  
Hct116 Cells

ABSTRACT Mutations in components of the Wnt signaling pathway initiate colorectal carcinogenesis by deregulating the β-catenin transcriptional coactivator. β-Catenin activation of one target in particular, the c-Myc proto-oncogene, is required for colon cancer pathogenesis. β-Catenin is known to regulate c-Myc expression via sequences upstream of the transcription start site. Here, we report that a more robust β-catenin binding region localizes 1.4 kb downstream from the c-Myc transcriptional stop site. This site was discovered using a genome-wide method for identifying transcription factor binding sites termed serial analysis of chromatin occupancy. Chromatin immunoprecipitation-scanning assays demonstrate that the 5′ enhancer and the 3′ binding element are the only β-catenin and TCF4 binding regions across the c-Myc locus. When placed downstream of a simian virus 40-driven promoter-luciferase construct, the 3′ element activated luciferase transcription when introduced into HCT116 cells. c-Myc transcription is negligible in quiescent HCT116 cells but is induced when cells reenter the cell cycle after the addition of mitogens. Using these cells, we found that β-catenin and TCF4 occupancy at the 3′ enhancer precede occupancy at the 5′ enhancer. Association of c-Jun, β-catenin, and TCF4 specifically with the downstream enhancer underlies mitogen stimulation of c-Myc transcription. Our findings indicate that a downstream enhancer element provides the principal regulation of c-Myc expression.

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