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p21(WAF1) gene promoter is epigenetically silenced by CTIP2 and SUV39H1

T Cherrier1, S Suzanne, L Redel

  • 1Université de Strasbourg, Institut de Virologie, France.

Oncogene
|July 8, 2009
PubMed

Insights

COUP-TF-interacting protein 2 (CTIP2) silences the cell cycle regulator p21 gene transcription by interacting with histone modifiers. CTIP2 cooperates with SUV39H1 and histone methylation to suppress p21, impacting HIV-1 latency.

Area of Science:

  • Molecular Biology
  • Epigenetics
  • Cell Cycle Regulation

Background:

  • The cyclin-dependent kinase inhibitor CDKN1A/p21(WAF1) (p21) is a key regulator of cell cycle arrest in response to DNA damage, senescence, and tumor suppression.
  • p21 is primarily regulated at the transcriptional level.

Purpose of the Study:

  • To investigate the role of COUP-TF-interacting protein 2 (CTIP2) in regulating p21 gene transcription.
  • To elucidate the mechanism by which CTIP2 silences p21.
  • To determine the involvement of CTIP2 in HIV-1 infection and latency.

Main Methods:

  • Chromatin immunoprecipitation assays to assess protein recruitment to the p21 gene promoter.
  • Treatment with the SUV39H1 inhibitor chaetocin.
  • Analysis of p21 gene expression and cell cycle arrest.
  • Investigation of CTIP2 and SUV39H1 interaction and recruitment.

Main Results:

  • CTIP2 is recruited to the p21 gene promoter and silences its transcription via interactions with histone deacetylases and methyltransferases.
  • Inhibition of SUV39H1 with chaetocin repressed H3K9 trimethylation, stimulated p21 expression, and induced cell cycle arrest.
  • CTIP2 and SUV39H1 cooperatively inhibit p21 transcription at the promoter.
  • CTIP2 abolishes Vpr-mediated p21 stimulation, contributing to HIV-1 latency.

Conclusions:

  • CTIP2 acts as a constitutive suppressor of p21 gene transcription.
  • CTIP2 collaborates with SUV39H1 and histone methylation to silence p21.
  • This mechanism plays a role in regulating cell cycle arrest and potentially contributes to HIV-1 latency.

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