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Related Experiment Videos

A single-point mutation in HCF causes temperature-sensitive cell-cycle arrest and disrupts VP16 function

H Goto1, S Motomura, A C Wilson

  • 1Department of Molecular Biology, Graduate School of Medical Science, Kyushu University, Higashi-ku, Fukuoka, Japan.

Genes & Development
|March 15, 1997
PubMed
Summary

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A mutation in the HCF protein causes hamster cells to stop dividing and alters gene expression. This single mutation affects both viral gene activation and cell cycle progression, revealing a dual role for HCF.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Virology

Background:

  • The tsBN67 hamster cell line exhibits temperature-sensitive proliferation arrest.
  • Arrested cells show gene expression patterns resembling serum starvation.
  • This phenotype is linked to a mutation in the HCF protein.

Purpose of the Study:

  • To investigate the molecular basis of the tsBN67 cell cycle arrest.
  • To understand the role of the HCF protein in both cellular and viral processes.

Main Methods:

  • Characterization of the tsBN67 temperature-sensitive cell line.
  • Genetic analysis of the HCF protein mutation (Pro134Ser).
  • Assessing the impact of the mutation on VP16-mediated transcription and cell cycle progression.

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Main Results:

  • A single missense mutation (Pro134Ser) in HCF causes the temperature-sensitive phenotype.
  • The mutated HCF protein fails to support VP16 activation of HSV immediate-early genes at nonpermissive temperatures.
  • The HCF mutation disrupts cell cycle progression.

Conclusions:

  • The HCF protein is essential for both VP16-dependent transcription and cell cycle progression.
  • A single point mutation in HCF has pleiotropic effects, impacting viral transcription and host cell proliferation.