Transcriptional interaction between retroviral long terminal repeats (LTRs)

Mechanism of 5′ LTR suppression and 3′ LTR promoter activation of c-myc in avian B-cell lymphomas

Cornelius F. Boerkoel, Hsing Jien Kung

Research output: Contribution to journalArticle

22 Citations (Scopus)

Abstract

Chicken syncytial viruses induce bursal lymphomas by integrating into the c-myc locus and activating myc expression by 3′ long terminal repeat (LTR) promoter insertion. In contrast to wild-type proviruses, in which transcription initiates predominantly in the 5′ LTR, these mny-associated proviruses exhibit a predominance of transcription from the 3′ LTR and little transcription from the 5′ LTR. Most of these proviruses contain deletions within the 5′ end of their genome that spare the 5′ LTR. We report the identification of a 0.3-kb viral leader sequence that modulates 5′ and 3′ LTR transcriptional activities. In the presence of this sequence, transcription from the 5′ LTR predominates, but in its absence, the 3′ LTR promoter becomes activated, resulting in a high level of myc expression. This viral sequence does not behave like a classical enhancer; it activates transcription only when located downstream from the promoter and in the sense orientation. In this regard, it resembles the recently described human immunodeficiency virus RNA enhancer. This study suggests that retroviruses contain internal sequences which directionally activate the 5′ LTR promoter to facilitate transcription of the viral genome and that deletion of these sequences is one step in the activation of the 3′ LTR of myc-associated proviruses in avian bursal lymphomas.

Original languageEnglish
Pages (from-to)4814-4823
Number of pages10
JournalJournal of Virology
Volume66
Issue number8
Publication statusPublished - Aug 1 1992
Externally publishedYes

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terminal repeat sequences
Terminal Repeat Sequences
B-Cell Lymphoma
lymphoma
B-lymphocytes
promoter regions
proviruses
Proviruses
transcription (genetics)
Lymphoma
Retroviridae
genome
Sequence Deletion
Viral Genome
Human immunodeficiency virus
5' untranslated regions
Chickens
HIV
Genome
RNA

ASJC Scopus subject areas

  • Immunology

Cite this

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title = "Transcriptional interaction between retroviral long terminal repeats (LTRs): Mechanism of 5′ LTR suppression and 3′ LTR promoter activation of c-myc in avian B-cell lymphomas",
abstract = "Chicken syncytial viruses induce bursal lymphomas by integrating into the c-myc locus and activating myc expression by 3′ long terminal repeat (LTR) promoter insertion. In contrast to wild-type proviruses, in which transcription initiates predominantly in the 5′ LTR, these mny-associated proviruses exhibit a predominance of transcription from the 3′ LTR and little transcription from the 5′ LTR. Most of these proviruses contain deletions within the 5′ end of their genome that spare the 5′ LTR. We report the identification of a 0.3-kb viral leader sequence that modulates 5′ and 3′ LTR transcriptional activities. In the presence of this sequence, transcription from the 5′ LTR predominates, but in its absence, the 3′ LTR promoter becomes activated, resulting in a high level of myc expression. This viral sequence does not behave like a classical enhancer; it activates transcription only when located downstream from the promoter and in the sense orientation. In this regard, it resembles the recently described human immunodeficiency virus RNA enhancer. This study suggests that retroviruses contain internal sequences which directionally activate the 5′ LTR promoter to facilitate transcription of the viral genome and that deletion of these sequences is one step in the activation of the 3′ LTR of myc-associated proviruses in avian bursal lymphomas.",
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AB - Chicken syncytial viruses induce bursal lymphomas by integrating into the c-myc locus and activating myc expression by 3′ long terminal repeat (LTR) promoter insertion. In contrast to wild-type proviruses, in which transcription initiates predominantly in the 5′ LTR, these mny-associated proviruses exhibit a predominance of transcription from the 3′ LTR and little transcription from the 5′ LTR. Most of these proviruses contain deletions within the 5′ end of their genome that spare the 5′ LTR. We report the identification of a 0.3-kb viral leader sequence that modulates 5′ and 3′ LTR transcriptional activities. In the presence of this sequence, transcription from the 5′ LTR predominates, but in its absence, the 3′ LTR promoter becomes activated, resulting in a high level of myc expression. This viral sequence does not behave like a classical enhancer; it activates transcription only when located downstream from the promoter and in the sense orientation. In this regard, it resembles the recently described human immunodeficiency virus RNA enhancer. This study suggests that retroviruses contain internal sequences which directionally activate the 5′ LTR promoter to facilitate transcription of the viral genome and that deletion of these sequences is one step in the activation of the 3′ LTR of myc-associated proviruses in avian bursal lymphomas.

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