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Protein kinase C inhibits formation of va gene transcription initiation complex

Timothy E Shannon1, Calvin B L James

  • 1Department of Biology, Francis Marion University, Florence, South Carolina 29501, USA.

In Vitro Cellular & Developmental Biology. Animal
|January 30, 2004
PubMed

Insights

Protein kinase C (PKC) activation disrupts adenovirus VA gene transcription by targeting transcription factor IIIB (TFIIIB). This leads to the sequestration or degradation of TATA-binding protein (TBP), inhibiting transcription initiation.

Area of Science:

  • Molecular Biology
  • Gene Regulation
  • Biochemistry

Background:

  • Protein kinase C (PKC) is a key signaling enzyme.
  • Polymerase III (pol III) transcribes essential small RNAs, including adenovirus VA genes.
  • PKC activation is known to affect gene transcription.

Purpose of the Study:

  • To investigate the mechanism by which PKC activation represses transcription of the adenovirus VA gene.
  • To identify the specific molecular targets of PKC in the transcription process.
  • To elucidate the role of transcription factor IIIB (TFIIIB) in PKC-mediated repression.

Main Methods:

  • In vitro transcription assays using VA and VA/EL plasmids.
  • Preincubation experiments to assess the timing of PKC activation relative to transcription complex formation.
  • Phosphocellulose fractionation of cell extracts to isolate and test transcription factors.
  • Rescue experiments using partially purified TFIIIB and purified TATA-binding protein (TBP).

Main Results:

  • PKC activation repressed transcription of the VA gene when added during or after template addition, but not when templates were preincubated.
  • PKC-induced repression was rescued by partially purified TFIIIB, indicating a target within this factor.
  • The TATA-binding protein (TBP), a component of TFIIIB, could substitute for crude TFIIIB in rescue experiments.
  • PKC activation appears to affect TBP, leading to the disruption of pol III transcription initiation.

Conclusions:

  • PKC activation disrupts pol III transcription initiation by targeting TFIIIB.
  • The TATA-binding protein (TBP) is a likely target of PKC-mediated repression.
  • PKC activation likely leads to TBP sequestration or degradation, inhibiting VA gene transcription.

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