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Repressing Gene Transcription by Redirecting Cellular Machinery with Chemical Epigenetic Modifiers
10:28

Repressing Gene Transcription by Redirecting Cellular Machinery with Chemical Epigenetic Modifiers

Published on: September 20, 2018

Gene repression by coactivator repulsion

K Senger1, M Merika, T Agalioti

  • 1Department of Biochemistry and Molecular Biophysics, Columbia University, New York, New York 10032, USA.

Molecular Cell
|November 25, 2000
PubMed

Insights

The IRF-2 oncoprotein represses virus-induced interferon-beta (IFN-beta) gene transcription through a novel mechanism. Deleting the IRF-2 gene enhances IFN-beta expression and cellular antiviral response.

Area of Science:

  • Immunology
  • Molecular Biology
  • Virology

Background:

  • Interferon-beta (IFN-beta) is crucial for antiviral immunity.
  • IRF-2 is an oncoprotein involved in gene regulation.

Purpose of the Study:

  • To elucidate the mechanism by which IRF-2 represses virus-induced IFN-beta gene transcription.
  • To investigate the impact of IRF-2 deletion on IFN-beta expression and antiviral response.

Main Methods:

  • Studied the recruitment of IRF-2 to IFN-beta enhancers during viral infection.
  • Investigated the role of a specific domain in IRF-2 in blocking transcription complex assembly.
  • Analyzed IFN-beta expression in IRF-2 gene-deleted cells post-viral infection.

Main Results:

  • IRF-2 is recruited to IFN-beta enhancers as part of the enhanceosome complex during viral infection.
  • IRF-2's specific domain prevents the recruitment of CBP-Pol II holoenzyme, inhibiting transcription.
  • Deletion of the IRF-2 gene significantly increases IFN-beta expression and the number of responsive cells.

Conclusions:

  • IRF-2 acts as a repressor of virus-induced IFN-beta transcription via a novel mechanism involving enhanceosome disruption.
  • IRF-2 deletion enhances the cellular antiviral response by promoting IFN-beta gene induction.

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