The Moloney leukemia retroviral long terminal repeat trans-activates AP- 1-inducible genes and AP-1 transcription factor binding

H. Weng, Sang-Yun Choi, D. V. Faller

Research output: Contribution to journalArticle

21 Citations (Scopus)

Abstract

Moloney murine leukemia virus (Mo-MuLV) is a thymotropic and leukemogenic retrovirus which causes T lymphomas. The long terminal repeat (LTR) of Mo- MuLV affects the regulation of a number of cellular genes, including collagenase IV, monocyte chemoattractant protein-1, and c-jun genes, all of which contain 12-O-tetradecanoylphorbol-13-acetate-responsive element consensus sites within their promoters. We report here that Mo-MuLV stimulates the collagenase IV gene through transcription factor AP-1, and that the expression of a subgenomic portion of Mo-MuLV LTR alone is sufficient for this effect. Transient or stable expression of the viral LTR increases cellular AP-1 DNA binding activity. The collagenase IV 12-O- tetradecanoylphorbol-13-acetate-responsive element consensus sequence was shown to be required for this trans-activation. Deletions or mutations of this consensus site which abolished AP-1 binding also abolished trans- activation by the LTR. Transient or stable transfection of the viral LTR into cells stimulated c-jun gene expression, suggesting one mechanism whereby the vital LTR may induce cellular AP-1 activity. Thus, the Mo-MuLV LTR, through activation of the transcription factor AP-1, is capable of regulating cellular gene expression, including the induction of proto-oncogenes. This activity may be relevant to the mechanisms whereby retroviruses which do not contain oncogenes induce neoplasia.

Original languageEnglish
Pages (from-to)13637-13644
Number of pages8
JournalJournal of Biological Chemistry
Volume270
Issue number23
DOIs
Publication statusPublished - 1995 Jan 1
Externally publishedYes

Fingerprint

Terminal Repeat Sequences
Transcription Factor AP-1
Leukemia
Moloney murine leukemia virus
Genes
Viruses
Collagenases
jun Genes
Chemical activation
Tetradecanoylphorbol Acetate
Retroviridae
Gene expression
Acetates
Gene Expression
Proto-Oncogenes
Chemokine CCL2
Sequence Deletion
Consensus Sequence
Oncogenes
Transfection

ASJC Scopus subject areas

  • Biochemistry

Cite this

The Moloney leukemia retroviral long terminal repeat trans-activates AP- 1-inducible genes and AP-1 transcription factor binding. / Weng, H.; Choi, Sang-Yun; Faller, D. V.

In: Journal of Biological Chemistry, Vol. 270, No. 23, 01.01.1995, p. 13637-13644.

Research output: Contribution to journalArticle

@article{f825e61a7992402e9056f56414b9213b,
title = "The Moloney leukemia retroviral long terminal repeat trans-activates AP- 1-inducible genes and AP-1 transcription factor binding",
abstract = "Moloney murine leukemia virus (Mo-MuLV) is a thymotropic and leukemogenic retrovirus which causes T lymphomas. The long terminal repeat (LTR) of Mo- MuLV affects the regulation of a number of cellular genes, including collagenase IV, monocyte chemoattractant protein-1, and c-jun genes, all of which contain 12-O-tetradecanoylphorbol-13-acetate-responsive element consensus sites within their promoters. We report here that Mo-MuLV stimulates the collagenase IV gene through transcription factor AP-1, and that the expression of a subgenomic portion of Mo-MuLV LTR alone is sufficient for this effect. Transient or stable expression of the viral LTR increases cellular AP-1 DNA binding activity. The collagenase IV 12-O- tetradecanoylphorbol-13-acetate-responsive element consensus sequence was shown to be required for this trans-activation. Deletions or mutations of this consensus site which abolished AP-1 binding also abolished trans- activation by the LTR. Transient or stable transfection of the viral LTR into cells stimulated c-jun gene expression, suggesting one mechanism whereby the vital LTR may induce cellular AP-1 activity. Thus, the Mo-MuLV LTR, through activation of the transcription factor AP-1, is capable of regulating cellular gene expression, including the induction of proto-oncogenes. This activity may be relevant to the mechanisms whereby retroviruses which do not contain oncogenes induce neoplasia.",
author = "H. Weng and Sang-Yun Choi and Faller, {D. V.}",
year = "1995",
month = "1",
day = "1",
doi = "10.1074/jbc.270.23.13637",
language = "English",
volume = "270",
pages = "13637--13644",
journal = "Journal of Biological Chemistry",
issn = "0021-9258",
publisher = "American Society for Biochemistry and Molecular Biology Inc.",
number = "23",

}

TY - JOUR

T1 - The Moloney leukemia retroviral long terminal repeat trans-activates AP- 1-inducible genes and AP-1 transcription factor binding

AU - Weng, H.

AU - Choi, Sang-Yun

AU - Faller, D. V.

PY - 1995/1/1

Y1 - 1995/1/1

N2 - Moloney murine leukemia virus (Mo-MuLV) is a thymotropic and leukemogenic retrovirus which causes T lymphomas. The long terminal repeat (LTR) of Mo- MuLV affects the regulation of a number of cellular genes, including collagenase IV, monocyte chemoattractant protein-1, and c-jun genes, all of which contain 12-O-tetradecanoylphorbol-13-acetate-responsive element consensus sites within their promoters. We report here that Mo-MuLV stimulates the collagenase IV gene through transcription factor AP-1, and that the expression of a subgenomic portion of Mo-MuLV LTR alone is sufficient for this effect. Transient or stable expression of the viral LTR increases cellular AP-1 DNA binding activity. The collagenase IV 12-O- tetradecanoylphorbol-13-acetate-responsive element consensus sequence was shown to be required for this trans-activation. Deletions or mutations of this consensus site which abolished AP-1 binding also abolished trans- activation by the LTR. Transient or stable transfection of the viral LTR into cells stimulated c-jun gene expression, suggesting one mechanism whereby the vital LTR may induce cellular AP-1 activity. Thus, the Mo-MuLV LTR, through activation of the transcription factor AP-1, is capable of regulating cellular gene expression, including the induction of proto-oncogenes. This activity may be relevant to the mechanisms whereby retroviruses which do not contain oncogenes induce neoplasia.

AB - Moloney murine leukemia virus (Mo-MuLV) is a thymotropic and leukemogenic retrovirus which causes T lymphomas. The long terminal repeat (LTR) of Mo- MuLV affects the regulation of a number of cellular genes, including collagenase IV, monocyte chemoattractant protein-1, and c-jun genes, all of which contain 12-O-tetradecanoylphorbol-13-acetate-responsive element consensus sites within their promoters. We report here that Mo-MuLV stimulates the collagenase IV gene through transcription factor AP-1, and that the expression of a subgenomic portion of Mo-MuLV LTR alone is sufficient for this effect. Transient or stable expression of the viral LTR increases cellular AP-1 DNA binding activity. The collagenase IV 12-O- tetradecanoylphorbol-13-acetate-responsive element consensus sequence was shown to be required for this trans-activation. Deletions or mutations of this consensus site which abolished AP-1 binding also abolished trans- activation by the LTR. Transient or stable transfection of the viral LTR into cells stimulated c-jun gene expression, suggesting one mechanism whereby the vital LTR may induce cellular AP-1 activity. Thus, the Mo-MuLV LTR, through activation of the transcription factor AP-1, is capable of regulating cellular gene expression, including the induction of proto-oncogenes. This activity may be relevant to the mechanisms whereby retroviruses which do not contain oncogenes induce neoplasia.

UR - http://www.scopus.com/inward/record.url?scp=0029067732&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0029067732&partnerID=8YFLogxK

U2 - 10.1074/jbc.270.23.13637

DO - 10.1074/jbc.270.23.13637

M3 - Article

C2 - 7775415

AN - SCOPUS:0029067732

VL - 270

SP - 13637

EP - 13644

JO - Journal of Biological Chemistry

JF - Journal of Biological Chemistry

SN - 0021-9258

IS - 23

ER -