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Human eukaryotic release factor 3a depletion causes cell cycle arrest at G1 phase through inhibition of the mTOR

Céline Chauvin1, Samia Salhi, Olivier Jean-Jean

  • 1Unité de Biochimie Cellulaire, UMR 7098 CNRS-Université Pierre et Marie Curie, 9 quai Saint-Bernard, 75252 Paris Cedex 05, France.

Molecular and Cellular Biology
|June 15, 2007
PubMed

Insights

Eukaryotic release factor 3a (eRF3a) depletion causes cell cycle arrest by inhibiting mTOR signaling, impacting translation rates. Its GTP-binding activity is crucial for cell cycle progression.

Area of Science:

  • Molecular Biology
  • Cell Biology

Background:

  • Eukaryotic release factor 3 (eRF3) is a GTPase involved in translation termination.
  • eRF3 is implicated in cell cycle regulation, cytoskeleton organization, and tumorigenesis.
  • Mammals express two eRF3 forms, eRF3a and eRF3b, with eRF3a being the primary translation termination factor.

Purpose of the Study:

  • To investigate the role of eRF3a in cell cycle progression.
  • To determine the specific domains and activities of eRF3a required for cell cycle regulation.

Main Methods:

  • Utilized short interfering RNAs (siRNAs) to deplete eRF3a.
  • Employed flow cytometry to analyze cell cycle progression.
  • Assessed global translation rates and mRNA polysome profiles.
  • Examined the phosphorylation status of mTOR pathway substrates (4E-BP1, S6K1).

Main Results:

  • eRF3a depletion induced a G1 cell cycle arrest.
  • GTP-binding activity of eRF3a, not its N-terminal domain, was essential for restoring G1-to-S-phase progression.
  • Global translation rate decreased, and mRNA polysome loading was reduced in eRF3a-depleted cells.
  • Key mTORC1 targets, 4E-BP1 and S6K1, were hypophosphorylated upon eRF3a depletion.

Conclusions:

  • eRF3a plays a critical role in regulating cell cycle progression.
  • The G1 arrest and reduced translation observed are linked to mTOR pathway inhibition.
  • eRF3a is identified as a component of the mTOR activity regulatory pathway.

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