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Related Experiment Videos

Two elements in the bovine leukemia virus long terminal repeat that regulate gene expression.

D Derse, J W Casey

    Science (New York, N.Y.)
    |March 21, 1986
    PubMed
    Summary

    Bovine leukemia virus (BLV) expression is regulated by two novel elements in its long terminal repeat (LTR). One element acts as a cell-specific enhancer, while another downstream sequence activates transcription independently of BLV infection.

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    Area of Science:

    • Virology
    • Molecular Biology
    • Gene Regulation

    Background:

    • Bovine leukemia virus (BLV) transcripts are typically undetectable in infected tissues.
    • The BLV long terminal repeat (LTR) acts as a transcriptional promoter, but its activity is restricted to BLV-infected cells.

    Purpose of the Study:

    • To identify and characterize regulatory elements within the BLV LTR that control viral gene expression.
    • To investigate the function of specific LTR regions in promoting transcription.

    Main Methods:

    • Deletion mapping of the BLV LTR to identify functional regions.
    • Coupling LTR sequences to a heterologous SV40 early promoter.
    • Monitoring transcriptional activity using transient expression of the bacterial chloramphenicol acetyltransferase (CAT) gene.

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    Main Results:

    • Two independent regulatory elements were identified in the BLV LTR.
    • A 75-bp fragment from the U3 region acted as a cell-specific enhancer, boosting transcription only in BLV-infected cells.
    • A 250-bp fragment from the R region, downstream of the RNA start site, activated transcription independently of BLV infection when placed immediately downstream.

    Conclusions:

    • BLV gene expression is regulated by a cell-specific enhancer element upstream of the core promoter.
    • A novel sequence downstream of the RNA initiation site in the BLV LTR contributes to viral gene regulation.
    • These findings elucidate key mechanisms controlling BLV replication and pathogenesis.