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TATA binding protein-associated CK2 transduces DNA damage signals to the RNA polymerase III transcriptional machinery

A Ghavidel1, M C Schultz

  • 1Department of Biochemistry, University of Alberta, Edmonton, Alberta, Canada T6G 2H7.

Cell
|September 12, 2001
PubMed

Insights

DNA damage represses RNA polymerase III transcription by downregulating TFIIIB. Protein kinase CK2 signals this stress, dissociating from TBP-CK2 complexes to inhibit transcription, thus protecting genome integrity.

Area of Science:

  • Molecular Biology
  • Gene Regulation
  • DNA Damage Response

Background:

  • RNA polymerase III (pol III) transcribes essential genes for cellular function.
  • TFIIIB is the core transcription factor for pol III.
  • Maintaining genome integrity is crucial for cell survival.

Purpose of the Study:

  • To elucidate the mechanism of pol III transcription repression following DNA damage.
  • To identify the signaling pathway involved in this stress response.

Main Methods:

  • Investigated the role of TFIIIB and protein kinase CK2 in pol III regulation.
  • Analyzed protein-protein interactions and complex formation using biochemical assays.
  • Assessed changes in pol III transcription activity under DNA-damaging conditions.

Main Results:

  • DNA damage leads to the downregulation of TFIIIB, repressing pol III transcription.
  • Protein kinase CK2 acts as a signal transducer in this pathway.
  • CK2 normally activates the TATA-binding protein (TBP) subunit of TFIIIB.
  • DNA damage causes dissociation of CK2 catalytic subunits from TBP-CK2 complexes, reducing CK2 activity and pol III transcription.

Conclusions:

  • CK2 is the terminal effector in a pathway that represses pol III transcription upon DNA damage.
  • This repression mechanism helps maintain genome integrity by limiting transcription of non-essential genes during stress.

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