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Brigitte David-Watine1

  • 1Institut Pasteur, CNRS URA2582, Groupe E3 Biologie Cellulaire du Noyau, Paris, France. brigitte.david-watine@pasteur.fr

Plos One
|August 4, 2011
PubMed
Abstract

Insights

Depleting the nuclear pore protein Tpr triggers cell cycle arrest and senescence, dependent on p53. Tpr also regulates nuclear export and SUMOylation.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Biochemistry

Background:

  • Tpr (Translocated promoter region) is a large coiled-coil protein within the nuclear basket of the nuclear pore complex.
  • Its diverse functions have been proposed across various species, from yeast to humans.

Purpose of the Study:

  • To investigate the role of Tpr in cellular processes beyond its known structural functions.
  • To elucidate the impact of Tpr depletion on cell cycle regulation, protein nuclear export, and SUMOylation.

Main Methods:

  • RNA interference (RNAi) was used to deplete Tpr levels in cells.
  • Cellular phenotypes, including cell cycle arrest and senescence, were analyzed.
  • Nuclear export of proteins and SUMOylation pathways were assessed.

Main Results:

  • Tpr depletion induced a G0-G1 cell cycle arrest, leading to a senescent-like phenotype dependent on p53.
  • Impairment of nuclear export sequence (NES)-dependent nuclear export of proteins was observed.
  • Tpr depletion affected the level and function of SUMO-protease SENP2, impacting SUMOylation at the nuclear pore and cellular SUMOylation.

Conclusions:

  • This study provides the first evidence that a nuclear pore component, Tpr, controls cellular senescence.
  • New roles for Tpr in regulating SUMO-1 conjugation at the nuclear pore are identified.
  • Direct confirmation of Tpr's involvement in the nuclear export of NES-proteins is established.

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