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Polyomavirus small T antigen transactivates genes by its ability to provoke the synthesis and the stabilization of

B Klucky1, E Wintersberger

  • 1Division of Molecular Biology, Department of Medical Biochemistry, MFPL, Medical University of Vienna, Vienna, Austria.

Oncogene
|April 18, 2007
PubMed

Insights

Polyomaviridae small T antigen (ST) drives cell cycle entry by activating MYC and related genes. ST targets protein phosphatase PP2A and kinases, influencing MYC-mediated transactivation and cell growth.

Area of Science:

  • Virology
  • Molecular Biology
  • Cell Biology

Background:

  • DNA tumor viruses, such as polyomaviridae, can induce quiescent cells to enter the cell cycle.
  • Viral proteins, specifically the large and small T antigens (ST) of polyomaviruses, are key drivers of this process.
  • ST interacts with protein phosphatase PP2A and dnaK-type chaperones, initiating S-phase induction.

Purpose of the Study:

  • To investigate the mechanism by which polyomavirus ST antigen induces S-phase.
  • To determine the role of the transcription factor MYC in ST-mediated gene transactivation.
  • To elucidate the involvement of signal transduction pathways and protein kinases in ST's effects.

Main Methods:

  • Microarray analysis to identify ST-induced genes.
  • Experimental validation of MYC's role in ST-mediated gene expression.
  • Analysis of kinase activity and phosphorylation states in the presence of ST.
  • Inhibition studies targeting kinases and MYC activity.

Main Results:

  • ST transactivates genes involved in S-phase induction, including the transcription factor MYC.
  • ST-induced genes are also MYC targets, suggesting a MYC-dependent pathway.
  • MYC-regulated genes are induced by ST with delayed kinetics compared to MYC itself.
  • ST promotes the active phosphorylation of kinases within MYC-regulating signal transduction pathways coordinated by PP2A.
  • Inhibition of these kinases or MYC activity impairs ST-mediated transactivation.

Conclusions:

  • Polyomavirus ST antigen utilizes MYC and associated signal transduction pathways to induce cell cycle progression.
  • ST directly influences key kinases and PP2A, leading to MYC activation and subsequent gene expression.
  • This mechanism highlights a viral strategy for manipulating host cell machinery to promote viral replication.

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