A transcript from the long terminal repeats of a murine retrovirus associated with trans activation of cellular genes

Sang-Yun Choi, D. V. Faller

Research output: Contribution to journalArticle

19 Citations (Scopus)

Abstract

Infection of human or murine cells with murine leukemia viruses rapidly increases the expression of a number of genes that belong to the immunoglobulin superfamily and are involved in T-lymphocyte activation, including the class I major histocompatibility complex antigens. We have reported recently that the long terminal repeat (LTR) of Moloney murine leukemia virus encodes a trans activator which induces transcription and expression of class I major histocompatibility complex genes and certain cytokine genes. The portion of the LTR responsible for trans activation was mapped by deletions to lie within the U3 region. We demonstrate here that a transcript is initiated within the U3 region and that its presence correlates with the trans-activating activity. Analysis of the LTR region reveals a potential internal promoter element for RNA polymerase III transcription within the U3 region. Studies with polymerase inhibitors suggest that this LTR transcript, designated let (LTR-encoded trans activator), is a product of RNA polymerase III. The mechanisms whereby RNA leukemia viruses cause lymphoid neoplasia after a long latent period have been extensively studied but are only partially understood. The region of the LTR identified here as being important in trans activation has recently been shown to be a critical determinant of the leukemogenicity and latency of Moloney murine leukemia virus. These findings suggest a novel mechanism of retrovirus-induced activation of cellular gene expression, potentially contributing to leukemogenesis.

Original languageEnglish
Pages (from-to)7054-7060
Number of pages7
JournalJournal of Virology
Volume69
Issue number11
Publication statusPublished - 1995 Jan 1
Externally publishedYes

Fingerprint

Terminal Repeat Sequences
Retroviridae
Transcriptional Activation
Moloney murine leukemia virus
RNA Polymerase III
Trans-Activators
Major Histocompatibility Complex
Genes
Murine Leukemia Viruses
Histocompatibility Antigens Class I
RNA Viruses
Lymphocyte Activation
Immunoglobulins
Leukemia
Cytokines
T-Lymphocytes
Gene Expression
Infection
Neoplasms

ASJC Scopus subject areas

  • Immunology

Cite this

A transcript from the long terminal repeats of a murine retrovirus associated with trans activation of cellular genes. / Choi, Sang-Yun; Faller, D. V.

In: Journal of Virology, Vol. 69, No. 11, 01.01.1995, p. 7054-7060.

Research output: Contribution to journalArticle

@article{0b4a423426b541a281daa05339abe183,
title = "A transcript from the long terminal repeats of a murine retrovirus associated with trans activation of cellular genes",
abstract = "Infection of human or murine cells with murine leukemia viruses rapidly increases the expression of a number of genes that belong to the immunoglobulin superfamily and are involved in T-lymphocyte activation, including the class I major histocompatibility complex antigens. We have reported recently that the long terminal repeat (LTR) of Moloney murine leukemia virus encodes a trans activator which induces transcription and expression of class I major histocompatibility complex genes and certain cytokine genes. The portion of the LTR responsible for trans activation was mapped by deletions to lie within the U3 region. We demonstrate here that a transcript is initiated within the U3 region and that its presence correlates with the trans-activating activity. Analysis of the LTR region reveals a potential internal promoter element for RNA polymerase III transcription within the U3 region. Studies with polymerase inhibitors suggest that this LTR transcript, designated let (LTR-encoded trans activator), is a product of RNA polymerase III. The mechanisms whereby RNA leukemia viruses cause lymphoid neoplasia after a long latent period have been extensively studied but are only partially understood. The region of the LTR identified here as being important in trans activation has recently been shown to be a critical determinant of the leukemogenicity and latency of Moloney murine leukemia virus. These findings suggest a novel mechanism of retrovirus-induced activation of cellular gene expression, potentially contributing to leukemogenesis.",
author = "Sang-Yun Choi and Faller, {D. V.}",
year = "1995",
month = "1",
day = "1",
language = "English",
volume = "69",
pages = "7054--7060",
journal = "Journal of Virology",
issn = "0022-538X",
publisher = "American Society for Microbiology",
number = "11",

}

TY - JOUR

T1 - A transcript from the long terminal repeats of a murine retrovirus associated with trans activation of cellular genes

AU - Choi, Sang-Yun

AU - Faller, D. V.

PY - 1995/1/1

Y1 - 1995/1/1

N2 - Infection of human or murine cells with murine leukemia viruses rapidly increases the expression of a number of genes that belong to the immunoglobulin superfamily and are involved in T-lymphocyte activation, including the class I major histocompatibility complex antigens. We have reported recently that the long terminal repeat (LTR) of Moloney murine leukemia virus encodes a trans activator which induces transcription and expression of class I major histocompatibility complex genes and certain cytokine genes. The portion of the LTR responsible for trans activation was mapped by deletions to lie within the U3 region. We demonstrate here that a transcript is initiated within the U3 region and that its presence correlates with the trans-activating activity. Analysis of the LTR region reveals a potential internal promoter element for RNA polymerase III transcription within the U3 region. Studies with polymerase inhibitors suggest that this LTR transcript, designated let (LTR-encoded trans activator), is a product of RNA polymerase III. The mechanisms whereby RNA leukemia viruses cause lymphoid neoplasia after a long latent period have been extensively studied but are only partially understood. The region of the LTR identified here as being important in trans activation has recently been shown to be a critical determinant of the leukemogenicity and latency of Moloney murine leukemia virus. These findings suggest a novel mechanism of retrovirus-induced activation of cellular gene expression, potentially contributing to leukemogenesis.

AB - Infection of human or murine cells with murine leukemia viruses rapidly increases the expression of a number of genes that belong to the immunoglobulin superfamily and are involved in T-lymphocyte activation, including the class I major histocompatibility complex antigens. We have reported recently that the long terminal repeat (LTR) of Moloney murine leukemia virus encodes a trans activator which induces transcription and expression of class I major histocompatibility complex genes and certain cytokine genes. The portion of the LTR responsible for trans activation was mapped by deletions to lie within the U3 region. We demonstrate here that a transcript is initiated within the U3 region and that its presence correlates with the trans-activating activity. Analysis of the LTR region reveals a potential internal promoter element for RNA polymerase III transcription within the U3 region. Studies with polymerase inhibitors suggest that this LTR transcript, designated let (LTR-encoded trans activator), is a product of RNA polymerase III. The mechanisms whereby RNA leukemia viruses cause lymphoid neoplasia after a long latent period have been extensively studied but are only partially understood. The region of the LTR identified here as being important in trans activation has recently been shown to be a critical determinant of the leukemogenicity and latency of Moloney murine leukemia virus. These findings suggest a novel mechanism of retrovirus-induced activation of cellular gene expression, potentially contributing to leukemogenesis.

UR - http://www.scopus.com/inward/record.url?scp=0028842881&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0028842881&partnerID=8YFLogxK

M3 - Article

C2 - 7474125

AN - SCOPUS:0028842881

VL - 69

SP - 7054

EP - 7060

JO - Journal of Virology

JF - Journal of Virology

SN - 0022-538X

IS - 11

ER -