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The transcription factor B-Myb is maintained in an inhibited state in target cells through its interaction with the

Xiaolin Li1, Donald P McDonnell

  • 1Department of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, North Carolina 27710, USA.

Molecular and Cellular Biology
|May 9, 2002
PubMed

Insights

Nuclear corepressors N-CoR and SMRT regulate the B-Myb transcription factor, which controls cell cycle genes. Phosphorylation by cdk2/cyclin A blocks this interaction, impacting gene expression.

Area of Science:

  • Molecular Biology
  • Cell Cycle Regulation
  • Transcription Factor Function

Background:

  • B-Myb transcription factor regulates cell cycle genes but its activity is repressed until G1-S phase.
  • The mechanism of B-Myb repression has remained largely unknown.
  • Previous studies showed B-Myb phosphorylation by cdk2/cyclin A enhances its activity.

Purpose of the Study:

  • To investigate the mechanism of B-Myb repression during the cell cycle.
  • To identify proteins that interact with B-Myb and regulate its activity.
  • To elucidate the role of nuclear corepressors in B-Myb function.

Main Methods:

  • Biochemical assays to detect protein interactions.
  • Cell-based assays to assess transcriptional activity.
  • Site-directed mutagenesis to study B-Myb mutants.

Main Results:

  • Nuclear corepressors N-CoR and SMRT interact with B-Myb.
  • B-Myb mutants unable to bind N-CoR show constitutive transcriptional activity.
  • Phosphorylation of B-Myb by cdk2/cyclin A inhibits N-CoR binding.
  • Mutating the corepressor binding site on B-Myb bypasses the need for phosphorylation.

Conclusions:

  • N-CoR and SMRT are novel regulators of B-Myb transcriptional activity.
  • The interaction between B-Myb and corepressors is a key mechanism for cell cycle repression.
  • Phosphorylation by cdk2/cyclin A releases B-Myb repression by blocking corepressor interaction.

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