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PLoS One. 2011;6(7):e22423. doi: 10.1371/journal.pone.0022423. Epub 2011 Jul 19.

Silencing nuclear pore protein Tpr elicits a senescent-like phenotype in cancer cells.

Author information

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

Abstract

BACKGROUND:

Tpr is a large coiled-coil protein located in the nuclear basket of the nuclear pore complex for which many different functions were proposed from yeast to human.

METHODOLOGY/PRINCIPAL FINDINGS:

Here we show that depletion of Tpr by RNA interference triggers G0-G1 arrest and ultimately induces a senescent-like phenotype dependent on the presence of p53. We also found that Tpr depletion impairs the NES [nuclear export sequence]-dependent nuclear export of proteins and causes partial co-depletion of Nup153. In addition Tpr depletion impacts on level and function of the SUMO-protease SENP2 thus affecting SUMOylation regulation at the nuclear pore and overall SUMOylation in the cell.

CONCLUSIONS:

Our data for the first time provide evidence that a nuclear pore component plays a role in controlling cellular senescence. Our findings also point to new roles for Tpr in the regulation of SUMO-1 conjugation at the nuclear pore and directly confirm Tpr involvement in the nuclear export of NES-proteins.

PMID:
21811608
PMCID:
PMC3139644
DOI:
10.1371/journal.pone.0022423
[Indexed for MEDLINE]
Free PMC Article

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