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.