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Tip60 degradation by adenovirus relieves transcriptional repression of viral transcriptional activator EIA

A Gupta1, S Jha, D A Engel

  • 1Department of Biochemistry and Molecular Genetics, University of Virginia, School of Medicine, Charlottesville, VA, USA.

Oncogene
|November 27, 2012
PubMed

Insights

Adenoviruses degrade the tumor suppressor Tip60 using viral proteins E1B55K and E4orf6. This degradation is crucial for efficient viral gene expression and host cell gene alterations.

Area of Science:

  • Virology
  • Molecular Biology
  • Cancer Research

Background:

  • Adenoviruses are double-stranded DNA viruses that can transform cells and cause tumors.
  • Host cells employ defense mechanisms against viral infection, including limiting gene expression and inducing cell death.
  • Adenoviruses counteract host defenses by abrogating the DNA damage response pathway.

Purpose of the Study:

  • To investigate the interaction between adenoviruses and the tumor suppressor Tip60.
  • To elucidate the mechanism by which adenoviruses manipulate cellular pathways for their replication.
  • To understand the role of Tip60 in adenovirus infection and host gene regulation.

Main Methods:

  • Investigated the degradation of Tip60 by adenovirus oncoproteins E1B55K and E4orf6.
  • Utilized proteasome-mediated pathway analysis.
  • Examined Tip60 binding to the adenovirus immediate early promoter and its effect on EIA gene expression.

Main Results:

  • Adenovirus oncoproteins E1B55K and E4orf6 mediate the proteasomal degradation of Tip60.
  • Tip60 binds to the adenovirus immediate early promoter and suppresses EIA gene expression.
  • Tip60's suppression of EIA is partly mediated by retaining the viral repressor pVII on the promoter.

Conclusions:

  • Degradation of Tip60 by adenoviral early proteins is essential for efficient viral early gene transcription.
  • Adenovirus-mediated degradation of Tip60 contributes to alterations in host cellular gene expression.
  • Tip60 serves as a critical host factor targeted by adenoviruses to facilitate viral replication and pathogenesis.

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