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Bcl-2 can promote p53-dependent senescence versus apoptosis without affecting the G1/S transition

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Rincheval, Vincent | Renaud, Flore | Lemaire, Christophe | Godefroy, Nelly | Trotot, Pascale | Boulo, Viviane | Mignotte, Bernard | Vayssière, Jean-Luc

Edité par CCSD ; Elsevier -

International audience. With the aim to identify events involved in the determination of p53-dependent apoptosis versus growth arrest, we used rat embryo fibroblasts expressing a temperature-sensitive mutant (tsA58) of the SV40 large tumour antigen (LT). Heat-inactivation of LT leads to p53 activation and commitment to a senescent-like state (REtsA15 cell line) or apoptosis (REtsAF cell line). We report that senescence is associated with high levels of the anti-apoptotic Bcl-2 protein and a cell cycle arrest in G1 phase, whereas ap-optosis is associated with low levels of Bcl-2 and a cell cycle arrest in G2 phase. Here we show that Bcl-2, which can inhibit apoptosis and proliferation, turns the apoptotic phenotype into a senescent-like phenotype in G2 phase. This result suggests that Bcl-2-dependent inhibition of apoptosis could be crucial for the commitment to replicative senescence, whereas its ability to inhibit G1 progression would not be required.

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