Document Detail


Analysis of the binding proteins and activity of the long terminal repeat of Moloney murine leukemia virus during differentiation of mouse embryonal carcinoma cells.
MedLine Citation:
PMID:  2033663     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Mouse embryonal carcinoma (EC) cell lines were established which carry the stably integrated chloramphenicol acetyltransferase (CAT) gene under the control of the transcriptional elements of the long terminal repeat (LTR) of Moloney murine leukemia virus. The activity of three elements of the stably integrated LTR was analyzed in undifferentiated EC cells (stable CAT assay). Results of the study are summarized as follows. (i) In the stable assay, the promoter region of the LTR was inactive in undifferentiated ECA2 and F9 cells, and the level of the activity was 10(-4) of that in NIH 3T3 cells. (ii) In contrast to the results of the transient assay, the enhancer was active in undifferentiated ECA2 cells and in F9 cells. It activated CAT activity more than 60-fold and about 8-fold in ECA2 cells and F9 cells, respectively. (iii) Suppression by ELP, the embryonal LTR-binding protein, was more pronounced in the stable assay than in the transient assay. These data suggest that, when compared with NIH 3T3 cells, a major factor for the inactivity of the LTR in EC cells is the inefficiency of the promoter in this assay. Transcriptional activity of the LTR was analyzed during the differentiation of EC cells. In the case of ECA2 cells, the magnitude of activation by the enhancer did not change during differentiation. The activity of the promoter increased about 10-fold, and the suppression by ELP became negligible 4 days after the induction of differentiation. Upon differentiation of F9 cells, the activity of the enhancer increased more than 300-fold, but the promoter remained inactive. The pattern of LTR-binding proteins also varied during the differentiation of EC cells. Our present data suggest that the activity of LTR elements as assayed by the stable assay differs from the activity as assayed by the transient assay. It also indicates that the activity of these elements exhibits cell-type-specific changes during the differentiation of EC cells.
Authors:
T Tsukiyama; O Niwa; K Yokoro
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of virology     Volume:  65     ISSN:  0022-538X     ISO Abbreviation:  J. Virol.     Publication Date:  1991 Jun 
Date Detail:
Created Date:  1991-06-26     Completed Date:  1991-06-26     Revised Date:  2009-11-18    
Medline Journal Info:
Nlm Unique ID:  0113724     Medline TA:  J Virol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  2979-86     Citation Subset:  IM    
Affiliation:
Department of Pathology, Hiroshima University, Japan.
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MeSH Terms
Descriptor/Qualifier:
Animals
Cell Transformation, Neoplastic
Chloramphenicol O-Acetyltransferase / metabolism
Gene Expression Regulation, Viral
Mice
Moloney murine leukemia virus / genetics*
Plasmids
Promoter Regions, Genetic
Repetitive Sequences, Nucleic Acid*
Teratoma / genetics*
Transcription, Genetic
Tumor Cells, Cultured
Chemical
Reg. No./Substance:
EC 2.3.1.28/Chloramphenicol O-Acetyltransferase
Comments/Corrections

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