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Related Experiment Videos

Tackling Tat.

J Karn1

  • 1MRC Laboratory of Molecular Biology, Hills Road, Cambridge, CB2 2QH, UK. karn@mrc-lmb.cam.ac.uk

Journal of Molecular Biology
|November 5, 1999
PubMed
Summary
This summary is machine-generated.

Human immunodeficiency virus transactivator protein (Tat) regulates viral gene expression by controlling transcription elongation. Tat recruits TAK kinase to hyperphosphorylate RNA polymerase II, enhancing viral transcription through TAR RNA interaction.

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Area of Science:

  • Molecular Biology
  • Virology
  • Gene Regulation

Background:

  • Cellular gene activation typically relies on transcription initiation control by DNA-binding proteins.
  • Human immunodeficiency virus (HIV) transactivator protein (Tat) uniquely regulates viral gene expression by controlling transcription elongation.
  • HIV transcription initiates efficiently but is impaired by poorly processive polymerases without Tat.

Purpose of the Study:

  • To elucidate the mechanism by which the HIV Tat protein activates transcriptional elongation.
  • To identify the cellular factors and interactions involved in Tat-mediated transactivation.
  • To understand the role of Tat-associated kinase (TAK) in HIV transcription.

Main Methods:

  • Investigated Tat's interaction with the TAR RNA element.

Related Experiment Videos

  • Studied the stimulation of Tat-associated kinase (TAK) by Tat-bound TAR RNA.
  • Utilized inactive CDK9 kinase mutants and kinase inhibitors to assess TAK's role in HIV transcription.
  • Examined the role of cyclin T1 in TAR RNA recognition and Tat complex formation.

    • Main Results:

    • Tat recruits TAK to the transcription machinery via TAR RNA, leading to RNA polymerase II hyperphosphorylation.
    • TAK, containing CDK9 kinase, is essential for HIV long terminal repeat transcriptional regulation.
    • Cyclin T1, a component of TAK, also participates in TAR RNA binding.
    • A functional apical loop in TAR RNA is crucial for Tat to form a ternary complex with TAR RNA and cyclin T1, indicating its role as a co-factor binding site.

    Conclusions:

    • HIV Tat protein activates viral transcription by promoting transcriptional elongation through the recruitment of TAK.
    • TAK, particularly CDK9, and its interaction with cyclin T1 and TAR RNA are critical for Tat-mediated transactivation.
    • The TAR RNA apical loop serves as a binding site for cellular co-factors essential for Tat function.