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Multiple mechanisms of transcriptional repression by YY1

K M Galvin1, Y Shi

  • 1Department of Pathology, Harvard Cancer Center, Harvard Medical School, Boston, Massachusetts 02115, USA.

Insights

The transcription factor YY1 uses its zinc fingers to repress gene activity. Researchers found YY1 acts as an activator-specific repressor, employing multiple mechanisms to control transcription based on the target activator.

Area of Science:

  • Molecular Biology
  • Gene Regulation
  • Transcription Factors

Background:

  • The transcription factor YY1 (Yin Yang 1) possesses a C-terminal repression domain composed of four GLI-Krüppel type zinc fingers.
  • Previous models proposed DNA-bending or activator-quenching as mechanisms for YY1-mediated repression, with potential involvement of p300 and CBP.

Purpose of the Study:

  • To investigate the mechanisms of YY1-mediated transcriptional repression.
  • To elucidate the specific roles of individual zinc fingers in YY1's DNA binding and repression functions.
  • To determine if YY1 acts as a general repressor or an activator-specific repressor.

Main Methods:

  • Structure-and-function analysis of YY1 mutants to assess DNA binding and repression.
  • Investigation of the interaction between YY1 and coactivators like p300.
  • Comparative analysis of YY1's repression of transcription directed by different activators (CTF-1, Sp1, CREB).

Main Results:

  • Zinc finger 2 of YY1 is crucial for both DNA binding and transcriptional repression.
  • The functions of DNA binding and repression by YY1 can be dissociated, arguing against a DNA-bending repression model.
  • Physical interaction with p300 is insufficient for repressing CREB-mediated transcription.
  • YY1 functions as an activator-specific repressor, utilizing distinct mechanisms for different activators.

Conclusions:

  • YY1 employs multiple, activator-specific mechanisms for transcriptional repression.
  • Repression of CTF-1 involves direct physical interaction with YY1.
  • Repression of Sp1 and CREB likely occurs by YY1 interfering with activator communication to the general transcription machinery.

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