Variation in transcriptional activity of enhancer deleted Rous sarcoma virus (RSV) LTR in eukaryotic cell types

1987 ◽  
Vol 15 (5) ◽  
pp. 954-955
Author(s):  
MAURICE TREACY ◽  
FINIAN MARTIN
Keyword(s):  
Rous Sarcoma Virus ◽  
Transcriptional Activity ◽  
Cell Types ◽  
Eukaryotic Cell ◽  
Rous Sarcoma ◽  
Sarcoma Virus

Correlation between phosphorylation of a 34,000-molecular-weight protein, pp60src-associated kinase activity, and tumorigenicity in transformed and revertant vole cells

1984 ◽  
Vol 4 (1) ◽  
pp. 212-215
Author(s):  
J F Nawrocki ◽  
A F Lau ◽  
A J Faras
Keyword(s):  
Molecular Weight ◽  
Rous Sarcoma Virus ◽  
Kinase Activity ◽  
Cell Types ◽  
Cell Protein ◽  
Protein Kinase Activity ◽  
Rous Sarcoma ◽  
Tumorigenic Potential ◽  
Sarcoma Virus ◽  
Weight Protein

The phosphorylation of a 34,000-molecular-weight (34K) cell protein, purported to be a substrate of the avian retrovirus pp60src-associated protein kinase activity, was compared in three types of Rous sarcoma virus-infected vole cells: fully transformed cells, partial revertants which are morphologically normal in appearance but retain their tumorigenic potential, and full revertants which are similar to normal vole cells in all parameters including a lack of tumorigenicity. Although similar amounts of 34K protein are present in all three cell types, phosphorylation of the 34K protein was significantly reduced in the full revertant cell type. The reduced phosphorylation occurred at the tyrosine residue.

scholarly journals Correlation between phosphorylation of a 34,000-molecular-weight protein, pp60src-associated kinase activity, and tumorigenicity in transformed and revertant vole cells.

1984 ◽  
Vol 4 (1) ◽  
pp. 212-215 ◽  
Author(s):  
J F Nawrocki ◽  
A F Lau ◽  
A J Faras
Keyword(s):  
Molecular Weight ◽  
Rous Sarcoma Virus ◽  
Kinase Activity ◽  
Cell Types ◽  
Cell Protein ◽  
Protein Kinase Activity ◽  
Rous Sarcoma ◽  
Tumorigenic Potential ◽  
Sarcoma Virus ◽  
Weight Protein

The phosphorylation of a 34,000-molecular-weight (34K) cell protein, purported to be a substrate of the avian retrovirus pp60src-associated protein kinase activity, was compared in three types of Rous sarcoma virus-infected vole cells: fully transformed cells, partial revertants which are morphologically normal in appearance but retain their tumorigenic potential, and full revertants which are similar to normal vole cells in all parameters including a lack of tumorigenicity. Although similar amounts of 34K protein are present in all three cell types, phosphorylation of the 34K protein was significantly reduced in the full revertant cell type. The reduced phosphorylation occurred at the tyrosine residue.

scholarly journals Role of the Transcription Start Site Core Region and Transcription Factor YY1 in Rous Sarcoma Virus Long Terminal Repeat Promoter Activity

1998 ◽  
Vol 72 (8) ◽  
pp. 6592-6601 ◽  
Author(s):  
Constance M. Mobley ◽  
Linda Sealy
Keyword(s):  
Transcription Factor ◽  
Transcription Start Site ◽  
Rous Sarcoma Virus ◽  
Promoter Activity ◽  
Transcriptional Activity ◽  
Start Site ◽  
Transcription Start ◽  
Rous Sarcoma ◽  
Sarcoma Virus ◽  
Transcription Factor Yy1

ABSTRACT The Rous sarcoma virus (RSV) long terminal repeat (LTR) contains a transcriptionally potent enhancer and promoter that functions in a variety of cell types. Previous studies have identified the viral sequences required for enhancer activity, and characterization of these elements has provided insight into the mechanism of RSV transcriptional activity. The objective of this study was to better define the RSV LTR promoter by examining the transcription start site core (TSSC) region. Deletion of the TSSC resulted in complete loss of transcriptional activity despite the presence of a functional TATA box, suggesting that the TSSC is required for viral expression. Homologies within the TSSC to the DNA binding motif of YY1 suggested that it might regulate promoter activity. YY1 has been shown to regulate transcription in some cellular genes and viral promoters by binding to sites overlapping the transcription start site. Gel shift assays using YY1 antibody identified YY1 as one of three complexes that bound to the TSSC. Mutation of the YY1 binding site reduced RSV transcriptional activity by more than 50%, suggesting that YY1, in addition to other TSSC-binding factors, regulates RSV transcription. Furthermore, in vitro transcription assays performed with Drosophila embryo extract (devoid of YY1 activity) showed decreased levels of RSV transcription, while transient transfection experiments overexpressing YY1 demonstrated that YY1 could transactivate the RSV LTR ∼6- to 7-fold. We propose that the TSSC plays a vital role in RSV transcription and that this function is partially carried out by the transcription factor YY1.

scholarly journals Functional analysis of the transcription control region located within the avian retroviral long terminal repeat.

1985 ◽  
Vol 5 (3) ◽  
pp. 438-447 ◽  
Author(s):  
B R Cullen ◽  
K Raymond ◽  
G Ju
Keyword(s):  
Long Terminal Repeat ◽  
Control Region ◽  
Rous Sarcoma Virus ◽  
Transcriptional Activity ◽  
Terminal Repeat ◽  
Transcription Control ◽  
Enhancer Element ◽  
Rous Sarcoma ◽  
Sarcoma Virus ◽  
Ltr Promoter

We used several quantitative assays of in vivo transient gene expression to dissect the elements within the Rous sarcoma virus long terminal repeat (LTR) which constitute the retroviral transcription control region. Site-directed deletion mutagenesis was used to locate and define the enhancer and promoter elements within the LTR. In addition, we inserted exogenous DNA fragments into the LTR to examine the effects of position and sequence on the activity of these LTR transcriptional elements. The Rous sarcoma virus enhancer element, which we propose is located entirely within the LTR, was shown to activate both the beta-globin and retroviral LTR promoters when located in cis. We observed a striking correlation between the degree of activation and the distance between the retroviral promoter and enhancer elements. The LTR promoter element mediated the activation effect of the enhancer element, as LTR deletion mutants containing only the enhancer and TATA box region expressed little activity. The promoter region encoded a low but significant level of transcriptional activity even in the absence of an enhancer. Overall LTR transcriptional activity declined sharply with increasing distance between the LTR promoter and initiator elements. These results shed light on both the importance of the spatial arrangement of the sequence elements within this eucaryotic transcription control region and on the functional interrelationship between these elements.

Characterization of a stable eukaryotic cell line expressing the rous sarcoma virus integrase

Virology ◽  
1992 ◽  
Vol 189 (2) ◽  
pp. 500-510 ◽  
Author(s):  
Steven R. Mumm ◽  
Paul J. Hippenmeyer ◽  
Duane P. Grandgenett
Keyword(s):  
Cell Line ◽  
Rous Sarcoma Virus ◽  
Eukaryotic Cell ◽  
Rous Sarcoma ◽  
Sarcoma Virus

Functional analysis of the transcription control region located within the avian retroviral long terminal repeat

1985 ◽  
Vol 5 (3) ◽  
pp. 438-447 ◽  
Author(s):  
B R Cullen ◽  
K Raymond ◽  
G Ju
Keyword(s):  
Long Terminal Repeat ◽  
Control Region ◽  
Rous Sarcoma Virus ◽  
Transcriptional Activity ◽  
Terminal Repeat ◽  
Transcription Control ◽  
Enhancer Element ◽  
Rous Sarcoma ◽  
Sarcoma Virus ◽  
Ltr Promoter

We used several quantitative assays of in vivo transient gene expression to dissect the elements within the Rous sarcoma virus long terminal repeat (LTR) which constitute the retroviral transcription control region. Site-directed deletion mutagenesis was used to locate and define the enhancer and promoter elements within the LTR. In addition, we inserted exogenous DNA fragments into the LTR to examine the effects of position and sequence on the activity of these LTR transcriptional elements. The Rous sarcoma virus enhancer element, which we propose is located entirely within the LTR, was shown to activate both the beta-globin and retroviral LTR promoters when located in cis. We observed a striking correlation between the degree of activation and the distance between the retroviral promoter and enhancer elements. The LTR promoter element mediated the activation effect of the enhancer element, as LTR deletion mutants containing only the enhancer and TATA box region expressed little activity. The promoter region encoded a low but significant level of transcriptional activity even in the absence of an enhancer. Overall LTR transcriptional activity declined sharply with increasing distance between the LTR promoter and initiator elements. These results shed light on both the importance of the spatial arrangement of the sequence elements within this eucaryotic transcription control region and on the functional interrelationship between these elements.

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